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Hantaan virus (HTNV) causes hemorrhagic fever with renal syndrome (HFRS), which is a zoonosis endemic in eastern Asia, especially in China. The reservoir host of HTNV is field mouse (Apodemus agraricus). The main manifestation of HFRS, including acute kidney injury, increases vascular permeability, and coagulation abnormalities. In this paper, we review the current knowledge of the pathogenesis of HFRS including virus factor, immunity factor and host genetic factors. Furthermore, the treatment and prevention will be discussed.

Purpose: The present study was designed to explore the significant biomarkers and pathway-related modules for predicting the effects of eribulin relative to paclitaxel in ovarian cancer., Methods: The gene expression data E-GEOD-50831 were downloaded from the European Bioinformatics Institute (EBI) database. Differentially expressed genes (DEGs) were screened. Subsequently, differential coexpression network was constructed. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and pathway-related modules mining were conducted. Topological centralities (degree, betweenness, closeness and stress) analyses for coexpression network and pathway-related modules were performed to explore hub genes and the most significant pathways. Then, we verified our findings in an independent sample set via RT-PCR and Western blotting., Results: Centralities results of ESCO1, CDC27and MCM4 ranked the top five. Moreover, among the top 10% hub genes, CDC27, MCM4 and SOS1 were pathway-enriched genes in two networks. A total of 5 and 6 pathway-related modules were obtained under two drugs treatment. Based analyses of degree, betweenness and other centralities, DNA replication pathway-related module was the most significant under paclitaxel treatment, while cell cycle pathway-related module was the most significant under eribulin treatment. RT-PCR and Western blotting results were consistent with the bioinformatics results. The expression level of MCM4 was remarkably decreased under eribulin treatment relative to paclitaxel., Conclusions: The inhibition of ovarian cancer growth by paclitaxel and eribulin might be connected with downregulation of cell cycle and DNA replication pathway. Moreover, MCM4 signature might be a potential biomarker to predict the effect of eribulin in ovarian cancer.

LaCeF3:Tb microcrystalline was synthesized by microemulsion method, oleic acid-assisted solvothermal method, ultrasonic-assisted solvothermal method separately. LaCeF₃:Tb microcrystalline synthesized by ultrasonic-assisted solvothermal method is rarely reported. Using X-ray diffraction (XRD), scanning electron microscope (SEM), fluorescence spectroscopy (PL) method such as the crystal phase, morphology and luminescence properties of the samples have been characterized. XRD results show that the crystallization product is good, microcrystalline and standard card PDF# 38-0452 (the six-party LaCeF₃) is corresponding, SEM images showing the product has uniform size and morphology, under 250 nm excitation nanoparticlesshows strong green light, the main emission peaks respectively belonged to ⁵D₄-->⁷F₆ (489 nm), ⁵D₄-->⁷F₅ (545 nm), ⁵D₄-->⁷F₄ (585 nm) and ⁵D₄-->⁷F₃ (621 nm) transition of Tb³⁺. Through LaCeF₃ and LaCeF₃:Tb spectral studies prove the existence of the Ce-Tb energy transfer. Calculated the critical doping concentration of Tb in LaCeF₃microcrystalline synthesized by different methods.

T-2 toxin is one of the mycotoxins, a group of type A trichothecenes produced by several fungal genera including Fusarium species, which may lead to the decrease of the testosterone secretion in the primary Leydig cells derived from the mouse testis. The previous study demonstrated the effects of T-2 toxin through direct decrease of the testosterone biosynthesis in the primary Leydig cells derived from the mouse testis. In this study, we further examined the direct biological effects of T-2 toxin on steroidogenesis production, primarily in Leydig cells of mice. Mature mouse Leydig cells were purified by Percoll gradient centrifugation and the cell purity was determined by 3β-hydroxysteroid dehydrogenase (3β-HSD) staining. To examine T-2 toxin-induced testosterone secretion decrease, we measured the transcription levels of 3 key steroidogenic enzymes and 5 enzyme activities including 3β-HSD-1, P450scc, StAR, CYP17A1, and 17β-HSD in T-2 toxin/human chorionicgonadotropin (hCG) co-treated cells. Our previous study showed that T-2 toxin (10(-7) M, 10(-8) M and 10(-9) M) significantly suppressed hCG (10 ng/ml)-induced testosterone secretion. The studies demonstrated that the suppressive effect is correlated with the decreases in the levels of transcription of 3β-HSD-1, P450scc, and StAR (P<0.05) and also in enzyme activities of 3β-HSD-1, P450scc, StAR, CYP17A1, and 17β-HSD (P<0.05)., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Objective: To analyze the expressions of Bcl-2, B7-H1, EGFR and VEGF in colorectal cancer for the further investigation of their correlations with the clinical pathological features of colorectal cancer., Method: Fresh colorectal cancer tissues and the expressions of Bcl-2, B7-H1, VEGF and EGFR in paraneoplastic normal mucosal tissues of 57 cases were tested by immunohistochemisty method, and the results were analyzed by SPSS10.0., Results: 1. Compared with paraneoplastic normal tissues, the expressions of Bcl-2 and B7-H1 in colorectal cancer tissues increased significantly with significant difference (P<0.05), while the expression of EGFR and VEGF in colorectal cancer tissues showed no significant difference with those in paraneoplastic normal tissue (P>0.05); 2. The correlation with clinical pathological features: there was significant difference of expression rates of EGFR between different genders (P<0.05); the expressions of BCL-2 and B7-H1 in colorectal cancer of the high- and medium- differentiated groups were significantly higher than those of the low-differentiated group, and the difference was significant (P<0.01); compared with the colorectal cancer patients without lymph node metastasis (Dukes stage A+B), the expression of B7-H1 in patients with lymph node metastasis (Dukes stage C+D) was significantly higher (P<0.05); 3. Within the high- and medium- differentiated colorectal cancer tissues, Bcl-2 expression rate in B7-H1 negative group was higher than the positive group with significant difference (P<0.01)., Conclusions: In colorectal carcinoma, Bcl-2, B7-H1, EGFR and VEGF were all expressed, independent from age and depth of invasion. However, the expression level of Bcl-2 and B7-H1 correlated with tissue differentiation, and the latter also had correlation with tumor staging. Meanwhile, the short-term follow-up showed that high expression of Bcl-2/B7-H1 existed in death cases. Therefore, the expression detection of Bcl-2, B7-H1 might provide a clear understanding of the biological behavior of colorectal cancer, and was important for the diagnosis, treatment and prognosis judgment of colorectal cancer.

Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine that regulates immune responses. IL-10 has also been shown to enhance antitumor CD8 + T-cell responses in tumor models although the underlying mechanisms are not fully understood. In this study, we used a series of genetic mouse models and the mouse plasmacytoma J558 model to investigate this issue. J558 tumors grew significantly faster in IL-10 -/- mice than in wild type (WT) mice, but similarly in IL-10 -/- Rag2 -/- and Rag2 -/- mice. Tumors from IL-10 -/- mice contained fewer IFN-γ-producing CD8 + and CD4 + T cells than tumors from WT mice. Strikingly, depletion of total CD4 + T cells, but not CD25 + cells, resulted in tumor eradication in IL-10 -/- mice. Adoptive transfer studies revealed that CD4 + T cells from IL-10 -/- mice exhibited more potent suppression of cytotoxic T lymphocyte (CTL)-mediated tumor rejection than their WT counterparts, and IL-10-deficient tumor-infiltrating CD4 + T cells expressed higher levels of PD-L1 and CTLA-4 inhibitory molecules. Although IL-10-deficient CD8 + T cells are not defective in activation and initial rejection of tumors, adoptive transfer studies using IL-10-deficient P1CTL transgenic T cells that recognize the tumor rejection antigen P1A reveal that IL-10 is required for long-term persistence of CTLs and control of tumor growth. Thus, we have found that IL-10 enhances antitumor CTL responses by inhibiting highly suppressive CD4 + T cells and promoting CTL persistence. These data have important implications for the design of immunotherapy for human cancer.

The synthesis of a series of aromatic amide-derived non-biaryl atropisomers with a phosphine group and multiple stereogenic centers is reported. The novel phosphine ligands exhibit high diastereo- and enantioselectivities (up to >99:1 d.r., 95-99 % ee) as well as yields in the silver-catalyzed asymmetric [3+2] cycloaddition of aldiminoesters with nitroalkenes, which provides a highly enantioselective strategy for the synthesis of optically pure nitro-substituted pyrrolidines. In addition, the experimental results with regard to the carbon stereogenic center as well as the amide stereochemistry confirmed the potential of hemilabile atropisomers as chiral ligand in catalytic asymmetric [3+2] cycloaddition reaction., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Epstein-Barr virus-induced gene 3 (EBI3) encoded protein can form heterodimers with IL-27P28, and IL-12P35 to form IL-27, and IL-35. However, IL-27 stimulates, whereas IL-35 inhibits antitumor T-cell responses. IL-27 also limits the Foxp3 + regulatory T cell (Treg) population, whereas IL-35 has been shown to expand Tregs and foster Treg suppressive functions. It remains unclear which group of forces are dominant during antitumor T-cell responses. In this study, we evaluated the tumor growth and antitumor T-cell responses in EBI3-deficient mice that lack both IL-27 and IL-35. We found that injecting B16 melanoma cells into EBI3-deficient C57BL/6 mice, or J558 plasmacytoma cells into EBI3-deficient BALB/c mice resulted in significantly increased tumor growth relative to those implanted in wild-type control mice. Tumors from EBI3-deficient mice contained significantly decreased proportions of CD8 + T cells and increased proportions of CD4 + FoxP3 + Treg cells as compared to those from EBI3-intact mice. Tumor-infiltrating T cells from EBI3-deficient mice were impaired in their capacity to produce IFNγ. Phenotypically, Tregs from EBI3-deficient mice were highly suppressive and produced IL-10 in the tumor microenvironment. Depletion of Tregs or inactivation of the IL-10 pathway significantly abrogated tumor growth enhancement in Ebi3 -/- mice. Finally, we showed that Ebi3 -/- mice administered a melanoma vaccine failed to mount a CD8 + T-cell response and the vaccine failed to confer tumor rejection in EBI3-deficient mice. Taken together, these results suggest that Ebi3 -/- mice show a phenotype of IL-27-deficiency rather than IL-35-deficiency during anti-tumor T-cell responses. Thus, our results suggest that endogenous IL-27 is critical for both spontaneous and vaccine-induced antitumor T-cell responses.

Accumulating evidences from animal studies have indicated that both endogenous and exogenous IL-27, an IL-12 family of cytokine, can increase antitumor T-cell activities and inhibit tumor growth. IL-27 can modulate Treg responses, and program effector T cells into a unique T-effector stem cell (TSEC) phenotype, which enhances T-cell survival in the tumor microenvironment. However, animal studies also suggest that IL-27 induces molecular pathways such as IL-10, PD-L1 and CD39, which may downregulate tumor-specific T-cell responses. In this review paper, we will discuss the Yin and Yang aspects of IL-27 in the induction of tumor-specific T-cell responses, and the potential impacts of these functions of IL-27 in the design of cancer immunotherapy.

Pot grown cotton plants were watered with saltwater (NaCl solutions of different concentrations), followed by a duration of progressive drought stress. The changes in plantlet growth, photosynthetic rate, chlorophyll fluorescence were measured, and the water status of the plantlets, such as relative water content, water potential, osmotic potential, the Na+ and K+ contents in leaves during drought were measured and analyzed, in order to get an insight into the role of Na+ played in the adaptation of cotton to drought stress. The results showed that the growth of the plantlets was significantly inhibited, the net photosynthetic rates were remarkably lowered by the drought stress, but the plant height, biomass, net photosynthetic rate and Fv/Fm values in the cotton plants watered with 25-100 mmol x L(-1) x NaCl solution under drought stress were significantly higher than those watered with water under the same intensity of drought stress. Meanwhile, the soil and leaf relative water content, cell turgor, Na+ concentration in plants watered with 25-100 mmol x L(-1) NaCl solution were all significantly higher compared with that of plants watered with water, but the plant water potential and tissue osmotic potential were significantly lower with the decrease in tissue osmotic potential significantly correlated with the Na+ content. These results indicated that the presence of a moderate amount of Na+ in the soil could improve the water status of both the soil and the cotton plants, accelerate the absorption and accumulation of Na+ in the roots, lower the tissue osmotic potential, thereby enhancing the suction force of water in plant for maintaining a high cell turgor to maintain a relatively higher photosynthetic rate and growth rate. In this sense, it was suggested that the existence of a certain amount of NaCl in soil could effectively alleviate the adverse effects of drought on cotton.

Background: The objective of this study was to explore the role of laboratory parameters as early indicators of severity and as effective predictors of prognosis in patients with hemorrhagic fever with renal syndrome (HFRS)., Methods: A total of 356 patients were enrolled in this study and were divided into mild, moderate, severe and critical types according to the clinical classification of HFRS. The levels of 12 routinely tested laboratory parameters during the acute stage among the four types were compared. The predictive values of the laboratory parameters for prognosis were analyzed, and a risk model for prognosis based upon the parameters was constructed., Results: The levels of white blood counts (WBC), platelets (PLT), aspartate aminotransferase (AST), albumin (ALB), blood urea nitrogen (BUN), serum creatinine (Scr), prothrombin time (PT) and activated partial thromboplastin time (APTT) demonstrated significant differences among the four types (p<0.001); WBC, AST, PT and fibrinogen (Fib) were major independent risk factors for death; WBC, AST, PT and Fib used in combination were better for predicting prognosis than single parameters used alone (p<0.001)., Conclusions: Some routinely tested laboratory parameters can be beneficial as early indicators of severity of HFRS. Using a combination of WBC, AST, PT and Fib to predict the outcome in patients with HFRS exhibited acceptable diagnostic capability.

DNA vaccination can generate both humoral and cellular immunity, resulting in potential prophylactic and therapeutic vaccines in variety of conditions, including hepatitis B virus (HBV) infection. Fusion of cytokine gene is one of the ways to increase the immunogenicity of DNA vaccine. Interleukin (IL)-21 has been demonstrated to play an immunomodulatory role in HBV infection. Thus, we aimed to investigate the ability of IL-21 in the regulation of middle version of HBV envelop protein (MS) DNA vaccine. Fusion plasmid encoding IL-21 linked with MS was constructed. Normal and HBV transgenic mice were immunized by plasmid. pcDNA-IL-21/S2S induced a comparable level of anti-HBs antibody and HBsAg-specific CD8+ T-cell response with pcDNA-S2S. Furthermore, the level of circulating HBsAg was decreased by induction of anti-HBs antibody and HBsAg-specific CD8+ T-cell response to both pcDNA-IL-21/S2S and pcDNA-S2S vaccination in HBV transgenic mice. Thus, immunization with DNA vaccine encoding HBV MS protein induced both T- and B-cell response by targeting the specific antigen. Furthermore, it was also revealed that MS DNA vaccination could break immune tolerance in HBV transgenic mice. But IL-21 did not strengthen immune response induced by HBV DNA immunization. Our study suggested that MS-expressing plasmid may be useful for both preventive and therapeutic methods in HBV infection. However, IL-21 does not improve the immunogenicity and efficacy of MS DNA vaccination, and thus may not be used as a therapeutic marker for chronic hepatitis B.

Objective: To study the clinical characteristics of pediatric hemorrhagic fever with renal syndrome (HFRS), and to improve its understanding so as to reduce the misdiagnosis., Methods: A retrospective analysis was performed on the clinical data of 26 children with HFRS between January 2009 and December 2012., Results: The age of disease onset was mainly distributed between 7 and 14 years (23 cases, 88%), and the male-to-female ratio was 1.89:l. The clinical manifestations of pediatric HFRS varied. The early symptoms resembled those of a cold, and in the course of HFRS, most patients developed digestive symptoms such as vomiting and abdominal pain. The laboratory examinations usually implicated platelet changes, and the imaging examinations revealed polyserous effusions. The prominent complication was myocardial injury., Conclusions: Pediatric HFRS mainly occurs in school-age children, more commonly in males. HFRS does not have typical clinical manifestations or symptoms, so it should be distinguished from cold or appendicitis at the early stage. When applying the fluid replacement therapy, the cardiac function should be carefully monitored in case of heart failure.

Interleukin-35 (IL-35), a cytokine from the Interleukin-12 cytokine family, has been considered as an anti-inflammatory cytokine which promotes tumor progression and tumor immune evasion. It has also been demonstrated that IL-35 is secreted by regulatory T cells. Recent mouse experiments have shown that IL-35 produced by cancer cells promotes tumor growth via enhancing myeloid cell accumulation and angiogenesis, and reducing the infiltration of activated CD8[Formula: see text] T cells into tumor microenvironment. In the present paper we develop a mathematical model based on these experimental results. We include in the model an anti-IL-35 drug as treatment. The extended model (with drug) is used to design protocols of anti-IL-35 injections for treatment of cancer. We find that with a fixed total amount of drug, continuous injection has better efficacy than intermittent injections in reducing the tumor load while the treatment is ongoing. We also find that the percentage of tumor reduction under anti-IL-35 treatment improves when the production of IL-35 by cancer is increased.

Purpose: Our goal is to test whether CS1 could be targeted by chimeric antigen receptor (CAR) T cells to treat multiple myeloma (MM)., Experimental Design: We generated a retroviral construct of a CS1-specific CAR and engineered primary human T cells expressing the CAR. We then tested the capacity of CS1-CAR T cells to eradicate human MM tumor cells in vitro, ex vivo, and in vivo using orthotopic MM xenograft mouse models., Results: In vitro, compared with mock-transduced T cells, upon recognizing CS1-positive MM cells, CS1-CAR-transduced T cells secreted more IFN-γ as well as interleukin (IL)-2, expressed higher levels of the activation marker CD69, showed higher capacity for degranulation, and displayed enhanced cytotoxicity. Ectopically forced expression of CS1 in MM cells with low CS1 expression enhanced recognition and killing by CAR T cells. Ex vivo, CS1-CAR T cells also showed similarly enhanced activities when responding to primary MM cells. More importantly, in orthotopic MM xenograft mouse models, adoptive transfer of human primary T cells expressing CS1-CAR efficiently suppressed the growth of human MM.1S and IM9 myeloma cells and significantly prolonged mouse survival., Conclusions: CS1 is a promising antigen that can be targeted by CAR-expressing T cells for treatment of MM., (©2014 American Association for Cancer Research.)

Haemangiopericytoma (HPC) is a vascular tumour which originates in the pericytes of vessels and therefore it may occur at any site, but it is very uncommon in the jaw. From January 2000 to December 2011, a retrospective analysis of nine consecutive patients with HPCJ was performed. There were five patients with a primary tumour and four patients with a recurrent tumour. Of the nine patients, eight were male and one female. Their ages ranged from 23 years to 51 years, with a median age of 38 years. The tumours were located in the mandible in six patients and in maxilla in three cases. The median course of disease was 7.6 months (range 2-12 months). All patients underwent surgery. Two patients had postoperative adjuvant radiotherapy, and two cases were given postoperative adjuvant chemotherapy. The median follow-up period was 49 months (10-101 months). One patient suffered from lumbar metastasis, while another case had metastasis at local and multiple distant sites, and eventually died. There was no local recurrence or metastasis in other seven cases. HPCJ are rare and the clinical characteristics are not specific. The first choice of treatment is radical surgery. Adjuvant radiotherapy may be effective to improve the prognosis of HPCJ., (Copyright © 2013 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd. All rights reserved.)

Background: Hemorrhagic fever with renal syndrome (HFRS) has become an important public health concern because of the high incidence and mortality rates, and limited treatment and vaccination. Until now, clinical studies on characteristics and outcomes in critical patients with HFRS have been limited. The aim of this study was to observe the clinical characteristics and cumulative proportions surviving and explore the predictive effects and risk factors for prognosis., Methods: A detailed retrospective analysis of clinical records for critical HFRS patients was conducted. The patients enrolled were treated in the centre for infectious diseases, Tangdu Hospital, between January 2008 and August 2012. The clinical characteristics between the survivors and non-survivors were compared by Student's t-test or Chi-square test. The risk clinical factors for prognosis were explored by logistic regression analysis. The predictive effects of prognosis in clinical and laboratory parameters were analyzed by receiver operating characteristic (ROC) curves. The cumulative proportions surviving at certain intervals in the critical patients were observed by Kaplan-Meier survival analysis., Results: Of the 75 patients enrolled, the cumulative proportion surviving was 70.7% at the second week interval, with a 28-day mortality rate of 36.3%. The non-survivors tended to have higher frequencies of agitation, dyspnea, conjunctival hemorrhage, coma, cardiac failure, acute respiratory distress syndrome (ARDS) and encephalopathy (P < .05). ARDS, conjunctival hemorrhage and coma were risk factors for death in the critical patients with HFRS. The non-survivors were found to have lower serum creatinine (Scr) levels (P < .001) and higher incidences of prolonged prothrombin time (PT) (P = .006), activated partial thromboplastin time (APTT) (P = .003) and elevated white blood cells (WBC) levels (P = .005), and the laboratory parameters mentioned above reached statistical significance for predicting prognosis (P < .05)., Conclusion: The high fatality in critical patients with HFRS underscores the importance of clinicians' alertness to the occurrence of potentially fatal complications and changes in biochemical status to ensure that timely and systematically supportive treatment can be initiated when necessary.

Aim: To explore the feasibility and oncologic outcomes of segmental jejunal resection on the left side of the mesenteric vessels in patients with tumors of the angle of Treitz using data from a single center., Methods: Thirteen patients with tumors of the angle of Treitz who underwent surgery at our institution were prospectively followed. A segmental jejunal resection on the left side of the mesenteric vessels was performed in all patients. Formalin-fixed and paraffin-embedded tumor samples were examined. The primary end point of this analysis was disease-free survival., Results: In this study, there were 8 males and 5 females (mean age, 50.1 years; range, 36-74 years). The mean tumor size was 8.1 cm (range, 3.2-15 cm). Histologic examination showed 11 gastrointestinal stromal tumors (GISTs) and 2 adenocarcinomas. Five of the GIST patients presented with potential low risk, and 6 presented with intermediate and high risk, according to the National Institutes of Health criteria. One potentially high-risk patient showed tumor progression at 46 mo and died 52 mo after surgery. One patient with locally advanced adenocarcinoma received neoadjuvant chemotherapy and adjuvant radiotherapy, but the disease progressed, and the patient died 9 mo after surgery. One GIST patient without progression died 16 mo after surgery because of a postoperative intestinal obstruction. The median overall survival rate was 84.6 mo, and the median disease-free survival rate was 94.5 mo., Conclusion: The overall survival of patients with tumors of the angle of Treitz was encouraging even when the tumor size was relatively large. A segmental resection on the left side of the mesenteric vessels is considered to be a reliable and curative option for tumors of the angle of Treitz.

Remote stereocontrol through conformational transmission along a carbon chain is highly important in synthetic systems and molecular architectures. In this work, the interactional reactivity between a remote silicon-based bulky group and an O-/N-containing functional group has been revealed and determined by lateral lithiation-substitution, desilylation, as well as desilylation-olefination with benzaldehyde. The results suggest considerable information transmission and steric hindrance that can be exploited for the controllable synthesis of atropisomeric molecules. Based on the remote steric effect of a functional group across the aromatic ring of an amide, the construction of isolable atropisomeric amides with functional groups, such as alcohol, amine, and olefin was successfully achieved. All these new atropisomers were obtained in reasonable yield in pure diastereomeric form, and the specific configuration of representative products was confirmed by X-ray crystallography., (© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Interleukin-12 is a pro-inflammatory cytokine which promotes Th1 and cytotoxic T lymphocyte activities, such as Interferon-[Formula: see text] secretion. For this reason Interleukin-12 could be a powerful therapeutic agent for cancer treatment. However, Interleukin-12 is also excessively toxic. Interleukin-27 is an immunoregulatory cytokine from the Interleukin-12 family, but it is not as toxic as Interleukin-12. In recent years, Interleukin-27 has been considered as a potential anti-tumor agent. Recent experiments in vitro and in vivo have shown that cancer cells transfected with IL-27 activate CD8+ T cells to promote the secretion of anti-tumor cytokines Interleukin-10, although, at the same time, IL-27 inhibits the secretion of Interferon-[Formula: see text] by CD8+ T cells. In the present paper we develop a mathematical model based on these experimental results. The model involves a dynamic network which includes tumor cells, CD8+ T cells and cytokines Interleukin-27, Interleukin-10 and Interferon-[Formula: see text]. Simulations of the model show how Interleukin-27 promotes CD8+ T cells to secrete Interleukin-10 to inhibit tumor growth. On the other hand Interleukin-27 inhibits the secretion of Interferon-[Formula: see text] by CD8+ T cells which somewhat diminishes the inhibition of tumor growth. Our numerical results are in qualitative agreement with experimental data. We use the model to design protocols of IL-27 injections for the treatment of cancer and find that, for some special types of cancer, with a fixed total amount of drug, within a certain range, continuous injection has better efficacy than intermittent injections in reducing the tumor load while the treatment is ongoing, although the decrease in tumor load is only temporary.

Brain ischemia and reperfusion activate the immune system. The abrupt development of brain ischemic lesions suggests that innate immune cells may shape the outcome of stroke. Natural killer (NK) cells are innate lymphocytes that can be swiftly mobilized during the earliest phases of immune responses, but their role during stroke remains unknown. Herein, we found that NK cells infiltrated the ischemic lesions of the human brain. In a mouse model of cerebral ischemia, ischemic neuron-derived fractalkine recruited NK cells, which subsequently determined the size of brain lesions in a T and B cell-independent manner. NK cell-mediated exacerbation of brain infarction occurred rapidly after ischemia via the disruption of NK cell tolerance, augmenting local inflammation and neuronal hyperactivity. Therefore, NK cells catalyzed neuronal death in the ischemic brain.

Hantaan virus (HTNV), which belongs to the genus Hantavirus, causes hemorrhagic fever with renal syndrome (HFRS) mainly in China. The diagnosis of HFRS depends on clinical manifestations and serological tests. A SYBR Green I based one-step real-time PCR assay was established in this study to detect HTNV. The HTNV standard curves were generated by plotting mean cycle threshold (Ct) values versus 10-fold serial dilutions of a previous titrated HTNV stock over a wide range of concentrations (1×10(7) to 1PFU/ml). The minimum detection limit of the assay was 1PFU/ml, and it was 100-fold more sensitive than conventional RT-PCR. Melting curve analysis indicated that there were no primer-dimers and non-specific products in the assay. No cross-reaction was observed with Seoul virus (SEOV). The specificity of the asssay was also verified by nuleotide sequencing of the PCR products. Intra- and inter-assay variability data were analyzed to examine the reproducibility of the assay. HTNV viral loads in HFRS patients were also investigated with the assay. These results indicated that the one-step real-time PCR assay is useful for detecting HTNV and for monitoring the viral loads., (Copyright © 2013 Elsevier B.V. All rights reserved.)

It is well known that the type III secretion system (T3SS) and type III (T3) effectors are essential for the pathogenicity of most bacterial phytopathogens and that the expression of T3SS and T3 effectors is suppressed in rich media but induced in minimal media and plants. To facilitate in-depth studies on T3SS and T3 effectors, it is crucial to establish a medium for T3 effector expression and secretion. Xanthomonas campestris pv. campestris (Xcc) is a model bacterium for studying plant-pathogen interactions. To date no medium for Xcc T3 effector secretion has been defined. Here, we compared four minimal media (MME, MMX, XVM2, and XOM2) which are reported for T3 expression induction in Xanthomonas spp. and found that MME is most efficient for expression and secretion of Xcc T3 effectors. By optimization of carbon and nitrogen sources and pH value based on MME, we established XCM1 medium, which is about 3 times stronger than MME for Xcc T3 effectors secretion. We further optimized the concentration of phosphate, calcium, and magnesium in XCM1 and found that XCM1 with a lower concentration of magnesium (renamed as XCM2) is about 10 times as efficient as XCM1 (meanwhile, about 30 times stronger than MME). Thus, we established an inducing medium XCM2 which is preferred for T3 effector secretion in Xcc.

Objectives: This study was conducted to measure the soft tissue of the alar base and the piriform aperture area of the maxillary bone of unilateral cleft lips with secondary nasal deformities when secondary operation are necessary to classify the alar base depression and to provide a clinical reference for the second surgery., Methods: Twenty-six patients with unilateral cleft lip with secondary nasal deformity were treated at the Department of Oral and Maxillofacial Surgery, School of Stomatology, China Medial University. Nose data were attained preoperatively and postoperatively. Correlations were made between the soft tissue and the bony depression and patient satisfaction with the nasi basis. Classifications were then made based on these data., Results: When the distance discrepancy of the bilateral piriform aperture depression was less than 4.5 mm, we obtained a fine appearance for the nose by repairing only the soft tissues. When it was more than 5 mm, we had to combine repair of the soft tissue with a bone graft or the restitution of the alveolar cleft. When the distance was between 4.5 mm and 5 mm, the surgeon considered both the wishes of the patient and the clinic's standard procedure., Conclusions: For patients with cleft lips and palates, the bony depression was not the only factor that resulted in postoperative alar depression. Anthropometry of the nose prior to surgery was important for choosing the methods that would yield satisfactory results.

Fanconi anemia complementation group F protein (FANCF) is a key factor, which maintains the function of FA/BRCA, a DNA damage response pathway. However, the functional role of FANCF in breast cancer has not been elucidated. We performed a specific FANCF-shRNA knockdown of endogenous FANCF in vitro. Cell viability was measured with a CCK-8 assay. DNA damage was assessed with an alkaline comet assay. Apoptosis, cell cycle, and drug accumulation were measured by flow cytometry. The expression levels of protein were determined by Western blot using specific antibodies. Based on these results, we used cell migration and invasion assays to demonstrate a crucial role for FANCF in those processes. FANCF shRNA effectively inhibited expression of FANCF. We found that proliferation of FANCF knockdown breast cancer cells (MCF-7 and MDA-MB-435S) was significantly inhibited, with cell cycle arrest in the S phase, induction of apoptosis, and DNA fragmentation. Inhibition of FANCF also resulted in decreased cell migration and invasion. In addition, FANCF knockdown enhanced sensitivity to doxorubicin in breast cancer cells. These results suggest that FANCF may be a potential target for molecular, therapeutic intervention in breast cancer.

Hantaan virus (HTNV) is a major zoonotic pathogen that causes hemorrhagic fever with renal syndrome (HFRS) in Asia, especially in China. Shaanxi province, which is located in northwest of China, is one of the areas in China most severely afflicted with HFRS epidemics annually. This study aims to establish a quantitative RT-PCR (qRT-PCR) assay to detect HTNV both in cell culture and clinical serum samples. We established a SYBR Green I-based one-step qRT-PCR assay that targets the S segment of the HTNV genome for rapid detection and quantification. The HTNV cRNA standards were constructed by in vitro transcription, and the copy numbers of the HTNV cRNA were quantified. Standard curve was generated by determining the mean cycle threshold (Ct) values versus 10-fold serial dilutions of the HTNV cRNA over a range of 1 × 10(8) to 1 × 10(3) copies/μl. The standard curve had a reaction efficiency of 102.1%, a correlation coefficient (R(2)) of 0.998, and a slope of -3.273. The coefficient of variation (CV) of the intra- and inter-assays ranged from 0.68% to 3.00% and from 0.86% to 3.21%, respectively. The cycle intervals of the qRT-PCR assay between each dilution ranged from 2.9 to 3.8 cycles, and the lowest detection limit of the qRT-PCR assay was 10 copies/μl. The assay exhibited high specificity that was confirmed by melting curve analysis, and no cross reaction with the Seoul virus (SEOV) and other viruses (HBV, HCV and HIV) was observed. HTNV RNA was also detected in the 27 serum samples of clinical HFRS patients using the assay, and the HTNV RNA viral load ranged from 2.06 × 10(1) to 1.95 × 10(5) copies/μl. The SYBR Green I-based one-step qRT-PCR assay is a sensitive, specific, reproducible, and simple method for detecting and quantifying HTNV in cell culture and clinical samples.

Aim: To investigate the stress-induced apoptosis of natural killer (NK) cells and the changes in their killing activity in mouse livers., Methods: A restraint stress model was established in mice. Flow cytometry was employed to measure the percentage of NK cells and the changes in their absolute number in mouse liver. The cytotoxicity of hepatic and splenic NK cells was assessed against YAC-1 target cells via a 4 h 51Cr-release assay., Results: The restraint stress stimulation induced the apoptosis of NK cells in the liver and the spleen, which decreased the cell number. The number and percentage of NK cells in the spleen decreased. However, the number of NK cells in the liver decreased, whereas the percentage of NK cells was significantly increased. The apoptosis of NK cells increased gradually with prolonged stress time, and the macrophage-1 (Mac-1)(+) NK cells were more susceptible to apoptosis than Mac-1(-) NK cells. Large numbers of Mac-1(-) NK cells in the liver, which are more resistant to stress-induced apoptosis, were observed than the Mac-1(-) NK cells in the spleen. The stress stimulation diminished the killing activity of NK cells in the spleen was significantly decreased, but the retention of numerous Mac-1(-) NK cells in the liver maintained the killing ability., Conclusion: Significant stress-induced apoptosis was observed among Mac-1(+) NK cells, but not Mac-1(-) NK cells in the mouse liver. Stress stimulation markedly decreased the killing activity of NK cells in the spleen but remained unchanged in the liver.

Breast cancer resistance protein (BCRP/ABCG2) specifically transports various chemotherapeutic agents and is involved in the development of multidrug resistance (MDR) in cancer cells. MicroRNAs (miRNAs) can play an important role in modulating the sensitivity of cancer cells to chemotherapeutic agents. Therefore, after confirming that BCRP was increased in the mitoxantrone (MX)-resistant MCF-7 breast cancer cell line MCF-7/MX compared with its parental sensitive MCF-7 cell line, we aimed to explore the miRNAs that regulate BCRP expression and sensitize breast cancer cells to chemotherapeutic agents. In the present study, bioinformatic analysis indicated that miR-487a was one of the miRNAs that could bind to the 3' untranslated region (3'UTR) of BCRP. Quantitative RT-PCR (qRT-PCR) analysis demonstrated that the expression of miR-487a was reduced in MCF-7/MX cells, and a luciferase reporter assay demonstrated that miR-487a directly bound to the 3'UTR of BCRP. Moreover, ectopic miR-487a down-regulated BCRP expression at the mRNA and protein levels, increasing the intracellular accumulation and cytotoxicity of MX in resistant MCF-7/MX breast cancer cells. Meanwhile, inhibition of miR-487a increased BCRP expression at the mRNA and protein levels and induced MX resistance in sensitive MCF-7 breast cancer cells. Furthermore, the reduced expression of BCRP and increased antitumor effects of MX were also detected in MCF-7/MX xenograft tumors treated with the miR-487a agmir. Thus, our results suggested that miR-487a can directly regulate BCRP expression and reverse chemotherapeutic drug resistance in a subset of breast cancers., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Cytotoxic T lymphocyte (CTL) response is a critical component of the immune response to tumors, therefore optimal induction of CTL responses to tumor antigens is highly desired for developing efficient cancer immunotherapy. IL-27 is a member of the IL-12 family of cytokines that is comprised of an IL-12 p40-related protein subunit, EBV-induced gene 3 (EBI3), and a p35-related subunit, p28. IL-27 functions through IL-27R and has been shown to have potent anti-tumor activity via activation of a variety of immune components, including anti-tumor CD8(+) T cell responses. However, the exact mechanisms of how IL-27 enhances anti-tumor CD8(+) T cell responses are not fully understood. In this paper we mainly discuss the evidences that suggest novel mechanisms by which IL-27 enhances anti-tumor CTL responses, including IL-27 inhibition of activation-induced cell death; the phenotypes of IL-27-stimulated CTLs; IL-27-induced CTL IL-10/IL-21 production and IL-27-mediated suppression of regulatory T cell responses. These evidences suggest that IL-27 may have a great potential to be utilized in boosting anti-tumor CTL responses in human cancer patients.

CD200 is a cell membrane protein that interacts with CD200 receptor (CD200R) of myeloid lineage cells. During tumor initiation and progression, CD200-positive tumor cells can interact with M1 and M2 macrophages through CD200-CD200R-compex, and downregulate IL-10 and IL-12 productions secreted primarily by M2 and M1 macrophages, respectively. In the tumor microenvironment, IL-10 inhibits the activation of cytotoxic T lymphocytes (CTL), while IL-12 enhances CTL activation. In this paper, we used a system approach to determine the combined effect of CD200-CD200R interaction on tumor proliferation by developing a mathematical model. We demonstrate that blocking CD200 on tumor cells may have opposite effects on tumor proliferation depending on the "affinity" of the macrophages to form the CD200-CD200R-complex with tumor cells. Our results help understanding the complexities of tumor microenvironment., (Published by Elsevier Ltd.)

Background/aim: There is very limited experience in the management of telbivudine (LdT)-associated virological breakthrough (VBT) and resistance in the treatment of chronic hepatitis B (CHB) patients, and the guideline recommendations are primitively based on the general principles of rescue therapy to nucleos(t)ide analog resistance. The aim of this study is to determine the effect of the addition of adefovir (ADV) in hepatitis B e antigen (HBeAg)-positive CHB patients with VBT or resistance to LdT., Methods: Thirty-seven CHB patients with confirmed VBT and 31 patients with genotypic resistance to LdT were enrolled and thereafter treated with a combination of LdT and ADV for 12 months., Results: Combination therapy was safe and the majority of patients tolerated the therapy. LdT+ADV led to rapid decreases in viral loads, and viral replications were persistently suppressed, with 2.17 (VBT) and 2.31 (resistance) log(10) copies/ml reductions 12 months after rescue therapy, respectively. The rates corresponding to virological and biochemical responses were similar between the two groups at the end of observations (70.3 vs. 74.2% for virological response, P=0.720; 64.0 vs. 65.5% for biochemical response, P=0.907). The cumulative rates of serological responses were higher in patients with VBT than in those with resistance (35.1 vs. 9.67% for HBeAg loss, P=0.014; 10.8 vs. 3.23% for HBeAg/anti-HBe seroconversion, P=0.233)., Conclusion: LdT and ADV combination therapy led to significant decreases in serum hepatitis B virus DNA levels and normalization of alanine aminotransferase levels in patients with VBT or genotypic resistance to LdT. This rescue strategy was also associated with a higher rate of HBeAg serological outcomes in patients with confirmed LdT-related VBT.

Objective: To study the feasibility and clinical value of 13th lymph nodes in predicting general lymph nodes metastases for periampullary carcinoma., Methods: A total of 77 patients with pathologically confirmed periampullary carcinoma were recruited. And 26 (18 males and 8 females, age 38-79 years) of them underwent Whipple procedures during which 1% methylene blue or nanogate carbon was injected into tumor bed. The other 51 patients as controls (33 males, 18 females, age 38-78 years) . The dyed 13th lymph nodes were biopsied. Then routine lymphadenectomy was performed and their pathological results were analyzed., Results: In the experimental group, the lymph node drainage area of cancer was identified. However, in contrast with 51 patients in the control group, the labeling of 13th lymph nodes did not significantly increase the number of cleaned lymph nodes (15.8 (3-54) vs 17.6 (6-40) , P = 0.460)., Conclusion: 13th lymph nodes are non-suitable as sentinels for predicting general lymph nodes metastases of periampullary carcinoma.

Lack of immunogenicity of cancer cells has been considered a major reason for their failure in induction of a tumor specific T cell response. In this paper, we present evidence that decitabine (DAC), a DNA methylation inhibitor that is currently used for the treatment of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML) and other malignant neoplasms, is capable of eliciting an anti-tumor cytotoxic T lymphocyte (CTL) response in mouse EL4 tumor model. C57BL/6 mice with established EL4 tumors were treated with DAC (1.0 mg/kg body weight) once daily for 5 days. We found that DAC treatment resulted in infiltration of IFN-γ producing T lymphocytes into tumors and caused tumor rejection. Depletion of CD8(+), but not CD4(+) T cells resumed tumor growth. DAC-induced CTL response appeared to be elicited by the induction of CD80 expression on tumor cells. Epigenetic evidence suggests that DAC induces CD80 expression in EL4 cells via demethylation of CpG dinucleotide sites in the promoter of CD80 gene. In addition, we also showed that a transient, low-dose DAC treatment can induce CD80 gene expression in a variety of human cancer cells. This study provides the first evidence that epigenetic modulation can induce the expression of a major T cell co-stimulatory molecule on cancer cells, which can overcome immune tolerance, and induce an efficient anti-tumor CTL response. The results have important implications in designing DAC-based cancer immunotherapy.

To study the chemical effect of direct current arc plasma igniter, the emission spectrum of plasma jet was measured, and the active particles produced by the interaction of plasma jet with atmospheric air were analyzed. The NO and CO volume fractions were measured quantificationally by smoke analyzer at the 8cm downstream the plasma igniter exit, and the changing law between arc current and NO, CO volume fractions was obtained. The results show that the plasma jet interacting with atmospheric air produced active particles (H, O, N), charged particles (O2 +, N2+), and excited particles (N2 (A3), N2 (B3), N2 (C3), N2 (a1), O2 (a1), O2 (b1)). The NO and CO volume fractions increased with rising of are current and feedstock argon flow rate.

In the present study, we downregulated FANCF expression by small interfering RNA (siRNA) in OVCAR ovarian cancer cells to address the effects of decreased FANCF expression on the function of the Fanconi anemia (FA)/breast cancer susceptibility gene (BRCA) pathway. Furthermore, we investigated whether this method increases the sensitivity of OVCAR3 cells to adriamycin (ADM) and the possible mechanism(s). We found that silencing of FANCF inactivated the FA/BRCA pathway by decreasing the monoubiquitination and focus formation of FANCD2 and reduced the function of the FA/BRCA pathway, resulting in the inhibition of cell proliferation, increased cell apoptosis and DNA damage in OVCAR3 cells. Moreover, we observed that silencing of FANCF enhanced the antiproliferative effect of ADM in OVCAR3 cells and increased ADM intracellular accumulation consequently sensitizing OVCAR3 cells to ADM. Furthermore, silencing of FANCF increased cell apoptosis of OVCAR3 cells which was caused by decreased mitochondrial membrane potential (MMP)-induced DNA damage, activated Jun N-terminal kinase (JNK), increased release of cytochrome c, increased expression of cleaved caspase-3 and poly(ADP-ribose) polymerase (PARP) dependent on JNK activation following treatment of ADM. Collectively, we confirm that silencing of FANCF sensitizes OVCAR3 ovarian cancer cells to ADM, suggesting that FANCF may serve as a potential target for therapeutic strategies in the treatment of ovarian cancer.

Telbivudine (LdT) has demonstrated potent antiviral activity in nucleos(t)ide analogue (NA)-naïve chronic hepatitis B patients (CHB), but data on its efficacy in NA-experienced patients are limited. The aim of this study was to investigate the effect of LdT in hepatitis B e antigen-positive CHB patients with poor response to initial adefovir dipivoxil (ADV). Forty-two CHB patients with HBV DNA > 4 log10  copies/mL after 12 months of ADV monotherapy were enroled in the study and thereafter treated with LdT 600 mg daily for 18 months. Telbivudine led to a rapid decrease in viral load, and viral replication was persistently suppressed with a reduction of 2.26 log10  copies/mL 18 months after LdT treatment. The rates corresponding to virological and biochemical response at the end of observation were 97.6% (41/42) and 65.8% (25/38), respectively. HBeAg loss was found in 30.8% (12/39) of patients, while HBeAg/anti-HBe seroconversion was found in 17.9% (7/39). Only one patient was detected to have LdT-associated mutation, and no severe adverse events were reported. Optimization therapy with LdT monotherapy may be a good choice for CHB patients with poor response to ADV, and switching to LdT may be the most cost-effective rescue therapeutic strategy for patients with poor response to initial ADV monotherapy., (© 2012 Blackwell Publishing Ltd.)

Objective: The aim of this study was to analyze the clinical management of hamartomas in the head and neck region (HNH)., Study Design: From January 1996 to December 2011, a retrospective analysis of 194 patients with HNH was performed. The preoperative examinations, surgical treatment, and prognosis were recorded and analyzed., Results: Of the 194 patients, 107 were male and 87 female. Their ages ranged from 1 month to 82 years with a mean of 33 years. The most common locations were the oral mucosa (68.6%) and head and neck skin (27.3%). The course of disease ranged from 1 to 264 months with a mean of 66 months. Routine laboratory examinations were within normal limits. All patients underwent surgical removal of the lesions and prognosis was good., Conclusions: The clinical characteristics of HNH are not specific, and the clinical manifestation is always the same for benign tumors. The first choice of treatment is surgical excision, which results in a good prognosis., (Copyright © 2013 Elsevier Inc. All rights reserved.)

IL-35 is a member of the IL-12 family of cytokines that is comprised of an IL-12 p35 subunit and an IL-12 p40-related protein subunit, EBV-induced gene 3 (EBI3). IL-35 functions through IL-35R and has a potent immune-suppressive activity. Although IL-35 was demonstrated to be produced by regulatory T cells, gene-expression analysis revealed that it is likely to have a wider distribution, including expression in cancer cells. In this study, we demonstrated that IL-35 is produced in human cancer tissues, such as large B cell lymphoma, nasopharyngeal carcinoma, and melanoma. To determine the roles of tumor-derived IL-35 in tumorigenesis and tumor immunity, we generated IL-35-producing plasmacytoma J558 and B16 melanoma cells and observed that the expression of IL-35 in cancer cells does not affect their growth and survival in vitro, but it stimulates tumorigenesis in both immune-competent and Rag1/2-deficient mice. Tumor-derived IL-35 increases CD11b(+)Gr1(+) myeloid cell accumulation in the tumor microenvironment and, thereby, promotes tumor angiogenesis. In immune-competent mice, spontaneous CTL responses to tumors are diminished. IL-35 does not directly inhibit tumor Ag-specific CD8(+) T cell activation, differentiation, and effector functions. However, IL-35-treated cancer cells had increased expression of gp130 and reduced sensitivity to CTL destruction. Thus, our study indicates novel functions for IL-35 in promoting tumor growth via the enhancement of myeloid cell accumulation, tumor angiogenesis, and suppression of tumor immunity.

The regeneration of bony defects of the mandible using free vascularized bone grafts has become a reliable procedure during the last few years. Various donor sites are available to provide vascularized bone grafts for mandibular reconstruction such as the fibula flap, the iliac flap, and the scapula flap; the fibula flap has become the most popular workhorse flap to reconstruct the lower jaw for extensive surgical defects. It is a challenge for head and neck reconstructive surgeons if the patient (mostly the manual worker) refuses to use fibular flap to reconstruct an extensive mandible defect or the patients have contraindication to harvest fibular flap. We have performed 7 cases using computer-aided design and computer-aided manufacturing prefabricated titanium mesh combined with autogenous iliac cancellous bone graft plus with/without boiled nontumorous mandible bone to reconstruct such cases. Primary wound healing was achieved in all patients without complication, and reconstructive complications were not observed during the follow-up period. The patients were satisfied with the results both esthetically and functionally. This preliminary clinical study and cases demonstrate that it is a feasible alternative method to reconstruct mandibular defects, especially when vascularized bone grafting is not available.

IL-27 is a member of the IL-12 family of cytokines that is comprised of an IL-12 p40-related protein subunit, EBV-induced gene 3, and a p35-related subunit, p28. IL-27 functions through IL-27R and has been shown to have potent antitumor activity via activation of a variety of cellular components, including antitumor CD8(+) T-cell responses. However, the exact mechanisms of how IL-27 enhances antitumor CD8(+) T-cell responses remain unclear. Here we show that IL-27 significantly enhances the survival of activated tumor antigen-specific CD8(+) T cells in vitro and in vivo, and programs tumor antigen-specific CD8(+) T cells into memory precursor-like effector cells, characterized by upregulation of Bcl-6, SOCS3, Sca-1, and IL-10. While STAT3 activation and the CTL survival-enhancing effects can be independent of CTL IL-10 production, we show here that IL-27-induced CTL IL-10 production contributes to memory precursor cell phenotype induction, CTL memory, and tumor rejection. Thus, IL-27 enhances antitumor CTL responses via programming tumor antigen-specific CD8(+) T cells into a unique memory precursor type of effector cells characterized by a greater survival advantage. Our results have important implications for designing immunotherapy against human cancer., (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Background: Postoperative hospital stay after pancreaticoduodenectomy (PD) is relatively longer than after other gastrointestinal operations. The aim of the current study was to investigate the risk factors associated with prolonged hospital stay after PD., Methods: Patients who had PD at the Cancer Hospital of Chinese Academy of Medical Sciences between December 2008 and November 2012 were selected for this retrospective study. Clinical and pathological data were collected and analyzed. The primary outcome was postoperative length of stay. Normal discharge or recovery was defined as a postoperative hospital stay of no more than 10 days; otherwise it was defined as delayed discharge or recovery (including hospital death)., Results: A total of 152 patients were enrolled in the present study. Postoperative hospital stay was (19.7 ± 7.7) days (range 7-57). Of the 152 patients, 67 were discharged within the normal time and 85 had delayed discharge. Postoperative complications occurred in 62.5% (95/152), and the mortality rate was 3.29% (5/152). Multiple regression analysis showed that delayed discharge was significantly associated with postoperative complications (adjusted odds ratio (OR) 10.40, 95% confidence interval (CI) 3.58-30.22), age (adjusted OR 4.09, 95% CI 1.16-14.39), body mass index (BMI) (adjusted OR 4.40, 95% CI 1.19-16.23), surgical procedure (adjusted OR 26.14, 95% CI 4.94-153.19), blood transfusion (adjusted OR 7.68, 95% CI 2.09-28.27), and fluid input (adjusted OR 3.47, 95% CI 1.24-11.57)., Conclusions: Postoperative complications increase the time to postoperative hospital discharge. The length of hospital stay after PD is also associated with age, BMI, blood transfusion, surgical procedure, and fluid input. Further studies with more patients are needed in future.

Although the role of CD14 in recognizing Mycobacterium tuberculosis is well-understood, the possible role of polymorphisms in susceptibility to develop tuberculosis remains unclear. This study evaluates whether there is an association of polymorphisms within the promoter of the CD14 gene with susceptibility to pulmonary tuberculosis. In a case-control study, we genotyped the eight known single nucleotide polymorphisms SNPs within the promoter of the CD14 gene of 698 Han Chinese subjects. Statistically significant differences between tuberculosis patients and healthy controls were found for G-1619A, T-1359G, A-1145G, and C-159T. The haplotype-GGGT, composed of these four SNPs, exhibited a significant association with the disease. Furthermore, expression levels of soluble CD14 were significantly higher in tuberculosis patients with the GGGT haplotype than with other haplotypes, while IgE expression levels were significantly reduced. Our results suggest that these four SNPs within the promoter of the CD14 gene are associated with susceptibility to pulmonary tuberculosis., (© 2012 John Wiley & Sons A/S.)

The innate immune response induced by Hantavirus is responsible for endothelial cell dysfunction and viral pathogenicity. Recent studies demonstrate that TLR4 expression is upregulated and mediates the secretion of several cytokines in Hantaan virus (HTNV)-infected endothelial cells. To examine viral interactions with host endothelial cells and characterize the innate antiviral responses associated with Toll-like receptors, we selected TLR4 as the target molecule to investigate anti-hantavirus immunity. TLR4 mRNA-silenced EVC-304 (EVC-304 TLR4-) cells and EVC-304 cells were used to investigate signaling molecules downstream of TLR4. The expression of the adaptor protein TRIF was higher in HTNV-infected EVC-304 cells than in EVC-304 TLR4- cells. However, there was no apparent difference in the expression of MyD88 in either cell line. The transcription factors for NF-κB and IRF-3 were translocated from the cytoplasm into the nucleus in HTNV-infected EVC-304 cells, but not in HTNV-infected EVC-304 TLR4- cells. Our results demonstrate that TLR4 may play an important role in the antiviral immunity of the host against HTNV infection through an MyD88-independent signaling pathway.

In a palladium-catalyzed oxidative esterification, hydrosilane can serve as an activator of palladium catalyst with bismuth, thus leading to a novel ligand- and silver-free palladium catalyst system for facile oxidative esterification of a variety of benzylic alcohols in good yields.

CD200 is a cell surface glycoprotein that has been implicated in a variety of human cancer cells and has been thought to play a pro-tumor role. However, in our recent study we have revealed that CD200 on cancer cells inhibits tumor formation and metastasis through inhibition of myeloid cells.

Photosynthesis is the unique source of energy for plant. Flag leaf contributed the majority of photosynthate after rice flowering. Ghd7 is a pleiotropic gene, which can significantly increase rice production. In order to study the genetic effects of Ghd7 on the flag leaf morphology, we made quantitative trait locus (QTL) analysis for flag leaf length (FLL), flag leaf width (FLW), and flag leaf area (FLA) using a Ghd7-BC2F2 population of 190 plants. In the BC2F2 population, the frequency distribution of FLL, FLW, and FLA were bimodal and in agreement with single Mendelian segregation ratio (3:1). FLL, FLW, and FLA were positively correlated with grains per panicle in the population. One QTL was mapped to the in-terval between markers RM3859 and C39 on chromosome 7, which explained 73.3%, 62.3%, and 71.8% of the variations for FLL, FLW, and FLA, and co-segregated with Ghd7. Two near-isogenic lines of NIL (mh7) and NIL (tq7) were devel-oped using Zhenshan 97 as the recurrent parent and Minghui 63 and Teqing as the donor parent, respectively. Both NILs significantly increased the phenotypic values of FLL, FLW, and FLA as compared with Zhenshan 97. FLL, The values of FLW and FLA for Ghd7 over-expression transgenic plants were 8.9 cm, 0.5 cm, and 17.8 cm2 larger than its recipient Heji-ang 19. These results demonstrated that Ghd7 plays an important role in controlling the flag leaf area in rice.

A highly efficient catalytic protocol for the isomerization of substituted amide-derived olefins is presented that successfully uses a hydride palladium catalyst system generated from [PdCl(2)(PPh(3))(2)] and HSi(OEt)(3). The Z to E isomerization was carried out smoothly and resulted in geometrically pure substituted olefins. Apart from the cis-trans isomerization of double bonds, the selective reduction of terminal olefins and activated alkenes was performed with excellent functional group tolerance in the presence of an amide-derived olefin ligand, and the products were obtained in high isolated yields (up to >99 %). Furthermore, the palladium/hydrosilane system was able to promote the reductive decarbonylation of benzoyl chloride when a (Z)-olefin with an aromatic amide moiety was used as a ligand., (Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Objective: To evaluate the value of sentinel lymph node biopsy in diagnosis of cervical metastasis in patients with early oral squamous cell carcinoma., Methods: Cochrane library, evidence-based medicine (EBM), PubMed, China national knowledge internet (CNKI) were searched for 2001 - 2011 literatures on sentinel lymph node biopsy in patients with oral squamous cell carcinoma as early diagnosis of cervical metastasis. The results were analysed by using Meta-analysis software Metadisc1.4., Results: There were 12 studies in which, a total of 793 patients with oral squamous cell carcinoma were involved in Meta-analysis. The combined sensitivity and specificity were 0.86 (95%CI: 0.81 - 0.90) and 0.99 (95%CI: 0.98 - 1.00) respectively., Conclusions: For early oral cancer patients, the sensitivity and specificity of sentinel lymph node biopsy are relatively high. The sentinel lymph node biopsy could be used to select which patients need neck dissection.

Hantaviruses infect human endothelial cells (ECs) and are known to cause vascular-permeability-based diseases, including hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). The αvβ3 integrins, which are highly expressed on the surface of ECs, serve as hantavirus receptors. Specifically, the β3 integrin and vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) form a functional complex and interact with each other. Signaling through this complex causes cytoskeletal reorganization, which is one of the most important mechanisms underlying hyperpermeability. In this study, we show that VEGF dramatically enhances Hantaan virus (HTNV)-directed permeability and increases the reorganization of the cytoskeleton and the disruption of junctional organizations in an EC monolayer at 3 days postinfection. HTNV infection reduced the effect of VEGF on adhesion, migration, and the upregulation of β3 expression, but the infection alone upregulated the expression of β3 and VEGFR2. These results indicate that in addition to its role in blocking β3 integrin activation as reported previously, HTNV blocks the function of the complex of VEGFR2 and β3 integrin, and the dysfunction of the complex may contribute to cytoskeletal reorganization in an HTNV-directed hyperpermeability response to VEGF.

Negative selection plays a key role in the clonal deletion of autoreactive T cells in the thymus. However, negative selection is incomplete; as high numbers of autoreactive T cells can be detected in normal individuals, mechanisms that regulate negative selection must exist. In this regard, we previously reported that CD24, a GPI-anchored glycoprotein, is required for thymic generation of autoreactive T lymphocytes. The CD24-deficient 2D2 TCR transgenic mice (2D2(+) CD24(-/-) ), whose TCR recognizes myelin oligodendrocyte glycoprotein (MOG), fail to generate functional 2D2 T cells. However, it was unclear if CD24 regulated negative selection, and if so, what cellular mechanisms were involved. Here, we show that elimination of MOG or Aire gene expression in 2D2(+) CD24(-/-) mice - through the creation of 2D2(+) CD24(-/-) MOG(-/-) or 2D2(+) CD24(/) ∼Aire(-/-) mice - completely restores thymic cellularity and function of 2D2 T cells. Restoration of CD24 expression on DCs, but not on thymocytes also partially restores 2D2 T-cell generation in 2D2(+) CD24(-/-) mice. Taken together, we propose that CD24 expression on thymic antigen-presenting cells (mTECs, DCs) down-regulates autoantigen-mediated clonal deletion of autoreactive thymocytes., (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)