Search

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, on p. 1969, two pairs of panels shown for the DU145 data appeared to contain overlaps, such that they may have been derived from the same original source (specifically, relating to the shCon and the shSMC1A experiments). The authors have referred back to their original data, and realize that inadvertent errors were made during the assembly of these figures. The corrected version of Fig. 5, showing discrete representative images for the shCon and the shSMC1A experiments with the DU145 cell line, is shown on the next page. All the authors agree to this corrigendum. Note that the revisions made to this figure do not adversely affect the results reported in the paper, or the conclusions stated therein. The authors regret that Fig. 5 was not presented in its correct form in their paper, thank the Editor of International Journal of Oncology for granting them the opportunity to publish this corrigendum, and offer their apologies to the Editor and to the readers of the Journal. [the original article was published in International Journal of Oncology 49: 1963-1972, 2016; DOI: 10.3892/ijo.2016.3697].

The diphenyl diselenide catalyzed oxidative degradation of benzoin to benzoic acid is reported. As this reaction can convert the malodorous compound into an odorless and innocuous product under mild conditions, it might be useful for pollutant disposal. The reaction does not require a transition-metal catalyst or a chemical oxidant, so that it can be performed at low cost and without generation of wastes. This is believed to be the first example of the use of organoselenium catalysis technology in pollutant destruction, thereby expanding its range of applications.

Background The benefit of targeted therapy for renal cell carcinoma (RCC) is largely crippled by drug resistance. Rapid disease progression and poor prognosis occur in patients with drug resistance. New treatments demand prompt exploration for clinical therapies. Ubiquitin-specific peptidase 39 (USP39) serves as the pro-tumor factor in several previous studies of other malignant tumors. To investigate the function and mechanism of USP39 in promoting malignant proliferation and angiogenesis of RCC. Methods We applied ONCOMINE database to analyze the correlation between USP39 expression level and the clinical characteristics of RCC. USP39 knockdown or overexpression plasmids were transfected into 786-O and ACHN cells. The HUVEC received cell supernatants of 786-O and ACHN cells with knockdown or overexpression USP39.The effect of USP39 on RCC was evaluated by MTT assay, cell cycle analysis, colony formation assay and tubule formation assay. The interaction between USP39 and VEGF-A alternative splicing was assessed by affinity purification and mass spectrometry, co-immunoprecipitation and Western blot assays. Results The mRNA expression level of USP39 in RCC was significantly higher than that in normal renal tissue (P (101–565) fragment directly mediated its binding to SRSF1 and SRPK1, and promoted the phosphorylation of SRSF1 to regulate VEGF-A alternative splicing. USP39 knockdown upregulated the expression of VEGF-A165b, and USP39 overexpression downregulated the expression of VEGF-A165b significantly (both P Conclusion USP39 acted as a pro-tumor factor by motivating the malignant biological processes of RCC, probably through inhibiting VEGF-A165b alternative splicing and regulating SRSF1 and SRPK1. USP39 may prove to be a potential therapeutic target for RCC. Graphic abstract

BackgroundMalignancy of the kidney is a rapidly progressive kidney disease and a major source of morbidity and mortality among people living with HIV (PLWH). Patients with HIV-associated kidey cancer experience higher cancer-specific mortality than the general population, and its mechanism remains poorly understood.MethodsTo heighten the awareness of kidney malignancy in patients with HIV infection to facilitate the early diagnosis of kidney cancer, we identified 2460 protein-coding transcripts in HIV-associated kidney cancer using comprehensive RNA sequencing (RNA-seq).ResultsKISS1R, CAIX, and NPTX2 mRNA expression levels were specifically increased in HIV-associated kidney cancer, and UMOD and TMEM213 mRNA were decreased in most cases based on real-time PCR analyses. These findings were similar to those noted for the general population with renal cell carcinoma. Immunohistochemical staining analysis also showed that a total of 16 of 18 kidney malignant cases among PLWH exhibited positive staining for KISS1R and CAIX.ConclusionPathway analysis of the differentially expressed mRNAs in HIV-associated kidney cancer revealed that several key pathways were involved, including voltage-gated chloride channel activity, distal tubule development, collecting duct development, fructose metabolic processes, and negative regulation of lipase activity. The identified molecular changes in kidney malignancy may offer a helpful explanation for cancer progression and open up new therapeutic avenues that may decrease mortality after a cancer diagnosis among PLWH.

Although the interaction between tumors and tumor-associated macrophages (TAMs) has been reported to facilitate the targeted drug resistance and progression of clear cell renal cell carcinoma (ccRCC), the related mechanisms remain unknown. Here, we report that SOX17 serves as a novel tumor suppressor in ccRCC and a positive regulatory loop, SOX17(low)/YAP/TEAD1/CCL5/CCR5/STAT3, facilitates the ccRCC-TAM interaction. SOX17 expression was commonly downregulated and negatively correlated with TAM infiltration in ccRCC specimens, and the integration of SOX17 and TAMs with the existing clinical indicators TNM stage or SSIGN score achieved better accuracy for predicting the prognosis of ccRCC patients. Mechanistically, SOX17 knockdown activated YAP signaling by promoting the transcription and nuclear distribution of YAP, which recruited TEAD1 to trigger CCL5 transcription. Then, CCL5 educated macrophages toward TAMs, which reciprocally enhanced ccRCC progression through CCL5/CCR5 and activated STAT3/SOX17(low)/YAP. However, SOX17 overexpression in ccRCC achieved the opposite effect. Thus, a positive regulatory loop, SOX17(low)/YAP/TEAD1/CCL5/CCR5/STAT3, was identified in the ccRCC-TAM interaction. Furthermore, targeting tumor-TAM interactions by blocking this positive regulatory network impaired the metastasis and targeted drug resistance of ccRCC in in vivo mouse models of lung metastasis and orthotopic ccRCC. These findings provide a new mechanism underlying the tumor-TAM interplay in ccRCC progression and present a potential target for inhibiting targeted drug resistance and metastasis in advanced ccRCC.

Background: Cancer stem cells (CSCs) are biologically characterized by self-renewal, multi-directional differentiation and infinite proliferation, inducing anti-tumor drug resistance and metastasis. In the present study, we attempted to depict the baseline landscape of CSC-mediated biological properties, knowing that it is vital for tumor evolution, anti-tumor drug selection and drug resistance against fatal malignancy. Methods: We performed single-cell RNA sequencing (scRNA-seq) analysis in 15208 cells from a pair of primary and metastatic sites of collecting duct renal cell carcinoma (CDRCC). Cell subpopulations were identified and characterized by t-SNE, RNA velocity, monocle and other computational methods. Statistical analysis of all single-cell sequencing data was performed in R and Python. Results: A CSC population of 1068 cells was identified and characterized, showing excellent differentiation and self-renewal properties. These CSCs positioned as a center of the differentiation process and transformed into CDRCC primary and metastatic cells in spatial and temporal order, and played a pivotal role in promoting the bone destruction process with a positive feedback loop in the bone metastasis microenvironment. In addition, CSC-specific marker genes BIRC5, PTTG1, CENPF and CDKN3 were observed to be correlated with poor prognosis of CDRCC. Finally, we pinpointed that PARP, PIGF, HDAC2, and FGFR inhibitors for effectively targeting CSCs may be the potential therapeutic strategies for CDRCC. Conclusion: The results of the present study may shed new light on the identification of CSCs, and help further understand the mechanism underlying drug resistance, differentiation and metastasis in human CDRCC.

Testicular cancer (TC) is the most common malignancy in men. Although the 5-year survival rate of TC patients exceeds 95%, the prognosis of patients with platinum-resistant tumors remains poor because of limited therapeutic options. Overcoming chemoresistance is the key to improving survival in poor-prognosis patients. However, the mechanism remains poorly understood. B-cell lymphoma 2 ovarian killer (BOK) is a proapoptotic protein and functions as a tumor suppressor in malignancy tumors. In this study, we found that BOK was frequently downregulated in TC tissues compared with paratumor tissues. BOK overexpression inhibited TC cell proliferation and invasion. In contrast, BOK knockdown promoted TC cell proliferation and invasion. Surprisingly, either BOK overexpression or knockdown rendered TC cells resistant to Cisplatin (DDP). In conclusion, BOK downregulation may be associated with tumorigenesis of TC. BOK had the potency to suppress TC cell proliferation and invasion, and may function as a tumor suppressor in TC. However, BOK also contributes to Cisplatin resistance. These data may provide a wider perspective on TC research and treatment.

Recent advances in immunotherapy are raising hope to treat clear cell renal cell carcinoma (ccRCC) with PD-L1 inhibitors, but only a small portion of patients are PD-L1 positive. The heterogeneous expression pattern of PD-L1 in patient population suggests that PD-L1 expression is under the control of diverse regulatory mechanisms. Although recent studies have identified numerous novel PD-L1 regulators, reports on microRNAs which modulate PD-L1 expression are much scarce. In this study, we confirmed that PD-L1 expression was up-regulated in ccRCC compared to paired normal tissues. Using miRDB and miRTarBase, 11 microRNAs were predicted to target PD-L1. After measuring the microRNA panel with TaqMan assays, we found that microRNA-497-5p down-regulation was associated with PD-L1 up-regulation. In TCGA-KIRC dataset, microRNA-497-5p down-regulation was also associated with PD-L1 up-regulation as well as shorter survival. We further validated that PD-L1 was a direct target of microRNA-497-5p in two RCC cell lines. In addition, microRNA-497-5p inhibited cell proliferation, clone formation and migration, while promoted apoptosis in in-vitro assays. Our study reveals a novel regulatory mechanism of PD-L1 expression and the potential of miR-497-5p as therapeutic target and biomarker deserves further investigation.

Asymmetric supercapacitors (ASCs) represent an effective electrochemical energy storage device with wider potential windows, which may lead to a substantial increase in the energy density and power density of the device. Unfortunately, their development is severely restricted by the carbon-based negative electrodes with low energy density. In this work, we demonstrate the facile synthesis of engineering WO3-x electrode on carbon cloth via hydrogenation, which achieves excellent electrochemical performance as a negative electrode for ASCs. The enhanced crystallinity and introduction of oxygen vacancy synergistically contribute to more reversible redox reactions, faster ion diffusion and charge transfer rates. The as-obtained WO3-x electrode reaches a high areal capacitance of 1.83 F cm−2 at 1 mA cm−2, and an outstanding electrochemical durability with high capacity retention of 74.8% after 10000 cycles. All these results open a new way to the construction of high-performance anodes for ASCs.

In order to clarify the co-research, research hotspots and knowledge evolution in the field of sustainable city, a visualization analysis of 1816 articles about sustainable city in the Web of Science was conducted by using bibliometrics method based on VOSviewer. The conclusions are listed as follows. (1) The citable documents of sustainable city have shown a rapid upward trend, with increasing attention and rising research hot spot, year by year, since 2015. (2) Scholars should strengthen the construction of global academic community, and China should be more extensive and in-depth cooperation with and scientific research institutions in European and American countries or regions. (3) The research dimension of sustainable city has been greatly expanding under the continuous development of complex algorithm, data science and artificial intelligence, Hence, the interdisciplinary characteristics of this research field, such as intersections, comprehensiveness and systematicness, are becoming increasingly prominent.

Recent reports have shown a rapid rise in the incidence of renal cell carcinoma (RCC), and Wnt (Wingless-related integration site) signaling pathway is important in RCC. Frizzled 8 (FZD8) is a member of Frizzled (FZD) receptor family which could activate canonical or non-canonical Wnt/β-catenin pathways. Nevertheless, the role of FZD8 in RCC is poorly investigated. The immunohistochemical analysis showed high expression of FZD8 in RCC tissues compared with peri-tumor tissues. FZD8 knockdown decreased the ability of proliferation and metastasis of RCC cells. Research revealed that the FZD8 regulated the transcription of Cyclin D1, c-Myc, and could promote the epithelial to mesenchymal transition (EMT) by mediating Vimentin and Snail through the Wnt/β-catenin signaling pathway. In addition, the results of our experiment revealed that FZD8 is involved in the regulation of non-canonical Wnt signaling pathway. These data suggested that the expression of FZD8 may play an important role in the proliferation and metastasis of RCC, and serve as a putative promising drug target for human RCC therapy.

Serine/threonine protein phosphatase 5 (PPP5C) is a member of the protein serine/threonine phosphatase family and has been shown to participate in multiple signaling cascades and tumor progression. We found that PPP5C was highly expressed in bladder cancer tissues compared to normal urothelial tissues, and positively correlated to tumor stages through ONCOMINE microarray data mining. Knockdown of PPP5C via a lentivirus-mediated short hairpin RNA (shRNA) markedly inhibited cell proliferation and colony formation. Flow cytometric analysis showed that PPP5C-deficient T24 and BT5637 bladder cancer cells were arrested in G0/G1 phase and induced apoptosis. In addition, tumor growth was inhibited in vivo in a xenograft nude mouse model. Further studies indicated that knockdown of PPP5C downregulated c-myc and CDK4, whereas upregulated p27, BAD and Beclin1. These results suggest that PPP5C is associated with bladder cancer (BCa) and plays an oncogenic role in the development and progression of bladder cancer.

Si-Shun Gan,* Jian-Qing Ye,* Lei Wang, Fa-Jun Qu, Chuan-Min Chu, Yi-Jun Tian, Wei Yang, Xin-Gang Cui Department of Urinary Surgery of Third Affiliated Hospital, Second Military Medical University, Shanghai, People’s Republic of China *These authors contributed equally to this work Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a protein expressed primarily in the liver, formerly known to maintain plasma lipid homeostasis by regulating low-density lipoprotein receptor levels, and its exact role in the radioresistance of prostate cancer (PCa) remains unclear. We aim to investigate the function of PCSK9 in the radioresistance of PCa cells.Methods: PCSK9 small interfering RNA (siRNA) was introduced into the PCa cells by transient transfection. Then, cells were exposed to ionizing radiation (IR) at indicated dose rates. Cell damage was detected using cell counting kit-8 (CCK-8) and Hoechest 33342/propidium iodide (PI) staining. Rhodamine-123 (Rho-123) dye was used to assay mitochondrial membrane potential alteration. Western blot was used to detect the apoptosis-related protein expression.Results: PCSK9 siRNA treatment significantly protected PCa cells from IR-induced cell damage, including enhancing cell viability, reducing apoptosis, and inhibiting MMPs. Moreover, PCSK9 siRNA repressed the increase of cytochrome C (cyto C), caspase-3, and B-cell leukemia/lymphoma 2 (Bcl-2)-associated X (Bax) expressions induced by IR and promoted Bcl-2 expression, which might partially interpret the radioprotective role of PCSK9 siRNA in PCa cells.Conclusion: PCSK9 might impact on radiosensitivity through mitochondrial pathways and serve as a novel therapeutic target for PCa patients. Keywords: PCSK9, prostate cancer, radioresistance, mitochondrial pathway

Prostate cancer (PRAD) is associated with abnormal cholesterol metabolism and low-density lipoprotein (LDL) receptor-related protein (LRP) family is essential for the homeostasis of cholesterol. Immune check points like PD-L1 are vital for tumour cells to evade immune attack. However, the potential cross-talk between these two pathways has not been explored before in PRAD. Insight from the regulation mechanism of PD-L1 in PRAD may help to optimise PD-L1 based immunotherapy. In this study, we investigated a regulation network of LRP11/β-catenin/PD-L1 in PRAD. We showed that the expression of LRP11 and PD-L1 was up-regulated in PRAD compared to paired normal tissues. LRP11 expression was positively correlated to PD-L1 expression in PRAD tissues. Further experiments in two PRAD cell lines with LRP11 over-expression and knockdown showed that LRP11 induced PD-L1 expression through β-catenin signalling. In addition, LRP11 over-expression in PRAD cell line induced immunosuppression of Jurkat cell in in-vitro co-culture system. The effects of LRP11 could be blocked by neutralising LRP11 or PD-L1 antibody. Our results provide evidence for a novel regulation mechanism of PD-L1 expression in PRAD and LRP11 may be a potential therapeutic target in PRAD.

BACKGROUND It is well known that lymphocytes play an important role in rheumatoid arthritis (RA). T cell immunoreceptors with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (TIGIT) have immunosuppressive co-stimulatory molecules that mediate inhibitory effects, but their roles in RA are poorly understood. MATERIAL AND METHODS Were recruited 76 patients with RA and 33 healthy controls (HC). Clinical manifestations, laboratory measurements, physical examination, and medical history of RA patients were recorded. The expression of TIGIT on CD3+ T lymphocytes, B lymphocytes, monocytes, neutrophils, CD3+CD4+ T lymphocytes, and CD3+CD8+ T lymphocytes was determined using flow cytometry. The expression of TIGIT on T lymphocytes in patients with RA was further analyzed to investigate its correlations with markers of autoimmune response, inflammation, and disease activity in RA. RESULTS Compared with HC, the expression levels of TIGIT on CD3+CD4+ T lymphocytes and CD3+CD8+ T lymphocytes were significantly increased in patients with RA (P < 0.01). The frequency of TIGIT-expressing CD3+CD4+ T lymphocytes was positively correlated with RF, increased ACPA, ESR, and CRP levels. The frequency of TIGIT-expressing CD3+CD8+ T lymphocytes was positively correlated with RF and ESR levels. Furthermore, the expression level of TIGIT on CD3+CD4+ T lymphocytes was positively correlated with the DAS28 score in RA. CONCLUSIONS The expression levels of TIGIT on T lymphocytes were elevated and correlated with disease activity in RA.

Structural maintenance of chromosome 1 alpha (SMC1A) gene has been reported to be related to tumor development in some types of human cancers. However, the misregulation of SMC1A and its functions in castration-resistant prostate cancer (CRPC) have not been well understood. In the present study, we found that SMC1A was elevated in androgen-independent PCa cell lines PC-3 and DU-145 compared to androgen sensitive LNCap and 22RV1 cells by qPCR and western blot assay. Knockdown of SMC1A inhibited cell growth, colony formation and cell migration abilities of PC-3 and DU145 cells by MTT, colony formation and transwell assays, and affected cell cycle progression in PC-3 and DU145 cells by flow cytometry. Moreover, SMC1A knockdown significantly reduced tumor growth in vivo in a nude mouse model. Additionally, we also found that the expression of SMC1A gene was higher in prostate cancer tissues than in the adjacent normal tissues by immunohistochemical staining, and was positively correlated to tumor metastasis and recurrence by Oncomine database mining. Taken together, the present study indicates that SMC1A may play an important role in malignant transformation of PCa under conditions of androgen deprivation and act as a new target for PCa diagnosis and treatment.

Human Ataxin-3 protein was first identified as a transcript from patients with Machado-Joseph disease (MJD), also known as spinocerebellar ataxia type 3 (SCA3). Recent studies have demonstrated that Ataxin-3 is involved in gastric cancer and lung cancer. However, the role of Ataxin-3 in testicular cancer (TC) remains poorly understood. This study aims to explore the significance of Ataxin-3 expression in TC. Firstly, we investigated 53 paired TC and para-tumor tissues and found that Ataxin-3 was overexpressed in TC tissues, and this overexpression of Ataxin-3 was correlated with tumor stages. Functionally, Ataxin-3 overexpression promoted cell proliferation, and Ataxin-3 knockdown inhibited cell proliferation. In addition, up-regulation of Ataxin-3 inhibited the expression of PTEN and activated the AKT/mTOR pathway. Conversely, inhibition of Ataxin-3 suppressed the expression of p-AKT and p-mTOR, and increased the expression of p-4EBP1. These findings may provide a better understanding about the mechanism of TC and suggest that Ataxin-3 may be a potential prognostic biomarker and therapeutic target for TC.

There are no effective therapies for advanced renal cell carcinoma (RCC), except for VEGFR inhibitors with only ~50% response rate. To identify novel targets and biomarkers for RCC is of great importance in treating RCC. In this study, we observed that eukaryotic initiation factor 3d (EIF3D) expression was significantly increased in RCC compared with paracarcinoma tissue using immunohistochemistry staining and western blot analysis. Furthermore, bioinformatics meta-analysis using ONCOMINE microarray datasets showed that EIF3D mRNA expressions in CCRCC tissue specimens were significantly higher than that in normal tissue specimens. In addition, RCC tissue microarray demonstrated that elevated EIF3D expression was positively correlated with TNM stage and tumor size. EIF3D silencing in human 786-O and ACHN CCRCC cell lines by RNA interference demonstrated that EIF3D knockdown obviously inhibited cell proliferation and colony formation, caused G2/M arrest through downregulation of Cyclin B1 and Cdk1 and upregulation of p21, and induced apoptosis shown by sub-G1 accumulation and RARP cleavage. Moreover, correlation analysis using ONCOMINE microarray datasets indicated that increased EIF3D mRNA expression was positively correlated to PCNA, Cyclin B1 and CDK1 mRNA expression in RCC. Collectively, these results provide reasonable evidences that EIF3D may function as a potential proto-oncogene that participates in the occurrence and progression of RCC.

// Yi Huang 1, 2, * , Xiu-Wu Pan 1, 3, * , Lin Li 1 , Lu Chen 1 , Xi Liu 1 , Jian-Lei Lu 4 , Xiao-Mei Zhu 4 , Hai Huang 1 , Qi-Wei Yang 1 , Jian-Qing Ye 3 , Si-Shun Gan 3 , Lin-Hui Wang 1 , Yi Hong 4 , Dan-Feng Xu 5 , Xin-Gang Cui 3 1 Department of Urinary Surgery of Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China 2 The 2nd Department of Oncology of Chenggong Hospital, Xiamen University, Xiamen, 361003, China 3 Department of Urinary Surgery of Third Affiliated Hospital, Second Military Medical University, Shanghai, 201805, China 4 R & D Departmemt of DuruoBiotechnologies Inc., Shanghai, 200233, China 5 Department of Urinary Surgery of Ruijin Hospital, Shanghai Jiaotong University, Shanghai, 200025, China * These authors have contributed equally to this work Correspondence to: Xin-Gang Cui, e-mail: xingangcui@126.com Dan-Feng Xu, e-mail: xu-danfeng@hotmail.com Yi Hong, e-mail: zandh@163.com Keywords: USP39, prostate cancer, prognosis, tumorigenesis, EGFR Received: January 15, 2016 Accepted: February 23, 2016 Published: March 03, 2016 ABSTRACT Castration resistance is a serious problem facing clinical treatment of prostate cancer (PCa). The underlying molecular mechanisms of acquired proliferation ability of tumor cells upon androgen deprivation are largely undetermined. In the present study, we identified that ubiquitin specific peptidase 39 (USP39) was significantly upregulated in PCa samples and cell lines. Elevated USP39 expression was positively correlated with Gleason score, predicted a poor outcome, and functioned as an independent risk factor for biochemical recurrence (BCR) especially in patients with a Gleason score ≤7. Our cell-based study showed that the expression level of USP39 was the highest in AR-negative PCa cell lines. Knockdown of USP39 in PCa cells inhibited cancer colony formation and tumor cell growth, and induced G2/M arrest and cell apoptosis. Microarray analysis suggested that knockdown of USP39 caused a reduced expression of EGFR. Silencing of USP39 inhibited the expression of EGFR 3′-end, and presented a remarkable block to the maturation of EGFR mRNA, suggesting that silencing of USP39 decreased the transcriptional elongation and maturation of EGFR mRNA. Oncomine datasets analysis showed that USP39 expression was positively correlated with EGFR level. The above findings suggest that USP39 plays a vital oncogenic role in the tumorigenesis of PCa and may prove to be a potential biomarker for predicting the prognosis of PCa patients.

It is well known that lymphocytes are important in rheumatoid arthritis (RA). Programmed cell death-1 (PD‑1) is one of the immunosuppressive costimulatory molecules, which mediates an inhibitory effect. However, its role in RA remains to be fully elucidated. In the present study, the expression levels of PD‑1 on T cells in the peripheral blood (PB) and synovial fluid (SF) were determined using flow cytometry. In addition, the expression levels of PD‑1 on T cells in the PB and SF of patients with RA were further analyzed to determine correlation with markers of the autoimmune response, inflammation and disease activity in RA. Compared with healthy controls, the expression of PD‑1 on T cells in the PB was significantly elevated in patients with RA (P

Abnormal expression of long non-coding RNA (lncRNA) has been demonstrated to be involved in a variety of human diseases. However, the role of lncRNA remains largely unknown in rheumatoid arthritis (RA). The present study aimed to investigate whether lncRNA are differentially expressed in RA. Differentially expressed lncRNA and mRNA in peripheral blood mononuclear cells from individuals with RA and healthy controls were detected using a human lncRNA microarray containing 30,586 lncRNA and 26,109 coding transcripts. Several candidate lncRNA and mRNA in 24 paired samples were verified by reverse transcription-quantitative polymerase chain reaction analysis. Bioinformatics analyses (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) were used to evaluate signaling pathways and biological functions influenced by the differentially expressed mRNA. A total of 5,045 lncRNA (upregulated, 2,410; downregulated, 2,635) and 3,289 mRNA (upregulated, 1,403; downregulated, 1,886) were differentially expressed in patients with RA (fold change >2; P

To analyze the expression profile of long non-coding RNA (lncRNA) in the lipopolysaecharide (LPS)-induced inflammation of monocyte-derived macrophages.Peripheral blood mononuclear cells were derived from healthy donor and induced into macrophages. The macrophages were divided into blank control group and LPS (1 mg/L) stimulated 12 hours group. Culture supernatants and cell pellets were harvested in each group, enzyme linked immunosorbent assay (ELISA) was used to assay the production changes of interleukins (IL-1β and IL-6), and tumor necrosis factor-α (TNF-α) in the supernatant. The technique of lncRNA microarray was used to test the lncRNA expression profile in LPS-induced inflammation of macrophages and control macrophages. The raw data of lncRNA were pretreated for normalization. Five lncRNA expressions were validated by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Furthermore, qRT-PCR was used to detect the expression of NR_028034 in macrophages after LPS-induced inflammation.(1) The contents of IL-1β (ng/L: 562.93±61.17 vs. 59.74±15.68), IL-6 (ng/L: 702.46±92.31 vs. 71.66±18.25) and TNF-α (ng/L: 794.50±63.89 vs. 85.12±22.07) in the LPS group were significantly higher than those in the blank control group (all P0.01). These results indicated that the inflammatory model of human macrophages was constructed successfully. (2) Compared with blank control group, and 1 479 lncRNA which have more than 2 folds variation and significant difference (P0.05) by statistical analysis was defined as lncRNA with differential expression. Among these lncRNA, LPS group showed 953 up- regulated and 526 down- regulated genes by 2 folds and 49 up- regulated and 35 down- regulated genes by 5 folds. (3) qRT-PCR results were generally consistent with the microarray data. (4) The expression of NR_028034 was increased by (4.41±0.65), (11.56±2.04), (18.58±1.36) folds compared with blank control group at 3, 6, 12 hours after LPS stimulation (all P0.01).These data show a significantly altered lncRNA expression profile in the LPS-induced inflammation of monocyte-derived macrophages, suggesting that lncRNA may be involved in regulation of macrophages inflammatory response.

Objectives It is well-known that lymphocytes play an important role in systemic lupus erythematosus (SLE). T cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory domains (TIGIT) is one of immunosuppressive costimulatory molecules that mediates an inhibitory effect. However, its roles in SLE are poorly understood. This study was designed to investigate the correlation between the frequencies of TIGIT-expressing CD3+CD4+ T lymphocytes and SLE. Methods Patients with SLE were recruited from the First Affiliated Hospital of Nanchang University. Medical history, clinical manifestations, physical examination and laboratory measurements were recorded. The expression of TIGIT on CD3+ T lymphocytes, B lymphocytes, monocytes, neutrophils, CD3+CD4+ T lymphocytes and CD3+CD8+ T lymphocytes were determined by flow cytometry. The frequencies of TIGIT-expressing CD3+CD4+ T lymphocytes in patients with SLE were further analyzed for correlations with markers of autoimmune response, inflammation, urine proteins and disease activity in SLE. Results The frequency of TIGIT-expressing CD3+CD4+ T lymphocytes was significantly elevated in SLE patients compared with healthy controls (P

Thousands of long noncoding RNAs (lncRNAs) have been reported and represent an important subset of pervasive genes associated with a broad range of biological functions. Abnormal expression levels of lncRNAs have been demonstrated in multiple types of human disease. However, the role of lncRNAs in systemic lupus erythematosus (SLE) remains poorly understood. In the present study, the expression patterns of lncRNAs and messenger RNAs (mRNAs) were investigated in peripheral blood mononuclear cells (PBMCs) in SLE using Human lncRNA Array v3.0 (8x60 K; Arraystar, Inc., Rockville, MD, USA). The microarray results indicated that 8,868 lncRNAs (3,657 upregulated and 5,211 downregulated) and 6,876 mRNAs (2,862 upregulated and 4,014 downregulated) were highly differentially expressed in SLE samples compared with the healthy group. Gene ontology (GO) analysis of lncRNA target prediction indicated the presence of 474 matched lncRNA‑mRNA pairs for 293 differentially expressed lncRNAs (fold change, ≥3.0) and 381 differentially expressed mRNAs (fold change, ≥3.0). The most enriched pathways were 'Transcriptional misregulation in cancer' and 'Valine, leucine and isoleucine degradation'. Furthermore, reverse transcription‑quantitative polymerase chain reaction data verified six abnormal lncRNAs and mRNAs in SLE. The results indicate that the lncRNA expression profile in SLE was significantly changed. In addition, a range of SLE‑associated lncRNAs were identified. Thus, the present results provide important insights regarding lncRNAs in the pathogenesis of SLE.

A facile and efficient synthesis route for the preparation of Bi–Fe–Co–Ni–Mn high entropy alloy films has been firstly reported in this work. The surface of the film is close-grained and the nanorods with high aspect ratios can be obtained by potentiostatic electrodeposition in the DMF (N,N-dimethylformamide)–CH3CN organic system. The effects of the deposition potential and the molar ratio of Bi(III) to transition metal ions (TMs(II)) in the organic system on the contents of Bi in the HE alloy were investigated. The annealed alloy structure is composed mainly of face-centered-cubic solid solution. The as-deposited alloys show soft magnetic behavior, and the annealed alloys exhibit hard magnetic properties.

Pd is investigated as electrocatalyst for 1-propanol and 2-propanol oxidation and compared with the conventional catalyst of Pt in alkaline medium. The results show that Pd is a good electrocatalyst for 1-propanol and 2-propanol oxidation. The oxidation reaction of 1-propanol and 2-propanol shows a very low activity on Pt electrode, however the oxidation reaction of 1-propanol and 2-propanol shows a high activity on Pd electrode in alkaline medium. The current densities of 1-propanol and 2-propanol oxidation on Pd electrode are much higher at corresponding potentials than that of methanol oxidation and the onset potentials of 1-propanol and 2-propanol oxidation on Pd electrode are more negative compared with that of methanol oxidation. The 1-propanol and 2-propanol oxidation on Pd electrode shows a stable performance. The results show that Pd can take the place of Pt for 1-propanol and 2-propanol oxidation in alkaline medium. The present study shows a promising choice of Pd as effective electrocatalyst for 1-propanol and 2-propanol electro-oxidation in alkaline medium.

Mycobacterium bovis BCG is known to have the capacity to inhibit the positioning of iNOS on BCG-containing phagosomes by interfering with EBP50, a scaffolding protein that controls the recruitment of inducible nitric oxide synthase (iNOS) at the vicinity of phagosomes in macrophages. However, knockdown of the expression of EBP50 still facilitates the intracellular survival of BCG, which suggested that EBP50 may have some other unknown antimycobacterial properties. In this study we show that overexpression of EBP50 by a recombinant lentivirus had no effect on the iNOS recruitment to M.tuberculosis-containing phagosomes, but significantly promoted the elimination of intracellular M.tuberculosis. We revealed in the present study that the enhancement of intracellular killing to M. tuberculosis upon EBP50 overexpression was due to the increased level of apoptosis in macrophages. We showed that EBP50 overexpression significantly increased the expression of iNOS and generation of nitric oxide (NO) and EBP50-induced apoptosis was NO-dependent and mediated by Bax and caspase-3. We found that M. tuberculosis decreases while Mycobacterium smegmatis increases the expression of EBP50 in RAW264.7 cells, which suggested that virulent mycobacteria are capable of modulating the antimycobacterial properties of macrophages by inhibiting the expression and interfering with the function of EBP50.

Macrophages display remarkable plasticity, with the ability to undergo dynamic transition between classically and alternatively activated phenotypes. Long non-coding RNAs (lncRNAs) are more than 200 nucleotides in length and play roles in various biological pathways. However, the role of lncRNAs in regulating macrophage polarization has yet to be explored. In this study, lncRNAs expression profiles were determined in human monocyte-derived macrophages (MDMs) incubated in conditions causing activation toward M(IFN-γ + LPS) or M(IL-4) phenotypes. Compared with primary MDMs, 9343 lncRNAs and 5903 mRNAs were deregulated in M(IFN-γ + LPS) group (fold change ≥2.0, P

Tuberculosis remains a global health problem caused by infection with Mycobacterium tuberculosis. Numerous studies have established a close correlation between the development of tuberculosis and the roles of neutrophils. Recently, a distinct population of CD15+ granulocytes was found to be present in the peripheral blood mononuclear cell (PBMC) fraction in humans. This population of granulocytes, termed low-density granulocytes (LDGs), was reported to be elevated and associated with disease activity or severity in a number of different conditions including SLE, asthma and HIV infection. However, both the frequency and clinical significance of LDGs associated with tuberculosis are unclear. Here we determined LDG levels and made comparisons between subjects with active pulmonary tuberculosis (PTB) and healthy controls, between PTB patients with mild-to-moderate disease and patients with advanced disease, and among PTB patients following anti-tuberculous therapy of varying durations. The direct correlation between M. tuberculosis infection and LDG levels was confirmed by in vitro infection of whole peripheral blood and isolated granulocytes with mycobacteria. Our results demonstrated that PBMCs in PTB patients contained significantly elevated percentages of LDGs compared with control subjects. LDGs in tuberculosis expressed higher levels of activation markers compared to normal-density granulocytes (NDGs). M. tuberculosis induced the generation of LDGs in both whole blood and isolated NDGs from control subjects, which suggests that LDGs associated with M. tuberculosis infection are likely to originate from in situ activation. Furthermore, our results revealed that the frequency of LDGs is associated with the severity of tuberculosis.

Pd and Au are investigated as electrocatalysts for 2-propanol oxidation and compared with the conventional catalyst of Pt in alkaline medium. The current density for 2-propanol oxidation on Pd electrode is much higher than that on Pt electrode. The onset potential for 2-propanol oxidation on Pd electrode is more negative compared with that on Pt electrode. The results show that Pd is a good electrocatalyst for 2-propanol oxidation and the activity for the electrooxidation of 2-propanol is higher than Pt and Au in alkaline medium. Pd has higher electrocatalytic activity and better stability for the electrooxidation of 2-propanol. The present study shows a promising choice of Pd as effective electrocatalyst for 2-propanol electrooxidation in alkaline medium. Keywords: Fuel cells, 2-Propanol electrooxidation, Palladium, Gold, Alkaline medium

Pd nanoparticles dispersed well on Ti were successfully prepared by the electrodeposition method used in this study. The results show that Pd has no activity for ethanol oxidation in acid media and is a good electrocatalyst for ethanol oxidation in alkaline media when the OH− concentration is greater than 0.001 M. The pH and ethanol concentration affects the ethanol oxidation. The reaction orders for OH− and ethanol are 0.2 and 1. The anodic transfer coefficient (α) is 0.1. The diffusion coefficient (D) of ethanol is calculated as 9.3 × 10−5 cm2 s−1 (298 K) when the concentration of KOH and ethanol is both 1.0 M. The overall rate equation for ethanol oxidation on Pd/Ti electrode in alkaline media is given as j = 1.4 × 10 - 4 C KOH 0.2 C ethanol exp 0.28 F RT η .

To assess the efficacy and tolerability of sunitinib dosing schedule of 2 weeks on and 1 week off (schedule 2/1) vs. the traditional schedule of 4 weeks on and 2 week off (schedule 4/2) and its influence on health-related quality of life (HRQoL) in Chinese patients with metastatic renal cell carcinoma (mRCC).A retrospective analysis of 108 patients with mRCC who were treated with sunitinib regimens (50mg daily) between January 2009 and July 2013 was undertaken. Overall, 3 groups of patients were studied according to the dosing schedule they received: schedule 4/2 (n = 50), transitional schedule 2/1 (T2/1; patients switched from schedule 4/2 to 2/1; n = 26), and initial schedule 2/1 (I2/1; n = 32). The tumor response, progression-free survival (PFS) time, adverse events, and HRQoL were assessed and compared among the groups.The incidences of diarrhea, fatigue, hand-foot syndrome, and neutropenia induced by the treatment of sunitinib were all significantly less common with schedule I2/1 and T2/1 than with schedule 4/2 (P0.05). Although there was no statistically significant difference in the tumor response among the 3 groups, the median PFS time was significantly longer with schedule I2/1 than with schedules T2/1 and 4/2 (11.2 vs. 9.4 and 9.5mo, respectively, P = 0.030), and HRQoL (as determined by 19-item Functional Assessment of Cancer Therapy Kidney Symptom Index scores) was better.Treatment with sunitinib 50mg daily using a 2/1 dosing schedule can provide better tolerability and a longer PFS with better HRQoL in Chinese patients with mRCC than the traditional schedule 4/2.

The tuberculous granuloma is an elaborately organized structure and one of the main histological hallmarks of tuberculosis. Macrophages, which are important immunologic effector and antigen-presenting cells, are the main cell type found in the tuberculous granuloma and have high plasticity. Macrophage polarization during bacterial infection has been elucidated in numerous recent studies; however, macrophage polarization during tuberculous granuloma formation and development has rarely been reported. It remains to be clarified whether differences in the activation status of macrophages affect granuloma formation. In this study, the variation in macrophage polarization during the formation and development of tuberculous granulomas was investigated in both sections of lung tissues from tuberculosis patients and an in vitro tuberculous granuloma model. The roles of macrophage polarization in this process were also investigated. Mycobacterium tuberculosis (M. tuberculosis) infection was found to induce monocyte-derived macrophage polarization. In the in vitro tuberculous granuloma model, macrophage transformation from M1 to M2 was observed over time following M. tuberculosis infection. M2 macrophages were found to predominate in both necrotic and non-necrotic granulomas from tuberculosis patients, while both M1 and M2 polarized macrophages were found in the non-granulomatous lung tissues. Furthermore, it was found that M1 macrophages promote granuloma formation and macrophage bactericidal activity in vitro, while M2 macrophages inhibit these effects. The findings of this study provide insights into the mechanism by which M. tuberculosis circumvents the host immune system as well as a theoretical foundation for the development of novel tuberculosis therapies based on reprogramming macrophage polarization.

A kind of crystal precursor, (NH4)5[(VO)6(CO3)4(OH)9]·10H2O, less than 12 × 40 μm in dimensions was synthesized by reaction of vanadyl dichloride and ammonium hydrocarbonate in solution. The precursor microcrystals were fined to less than 10 μm with mean size of about 4 μm, by using organic solvents and surfactant in the process of the synthetical technique. Thermolysis of the precursor in a flow of nitrogen gas was investigated by TGA and DTA. The XRD powders patterns for the products from the thermolysis of the precursor show that the VO2 powder obtained at 350, 365, 380 and 410°C for 30 min were a noncrystalline phase, a monoclinic one named as B phase, a mixed phase of the B and the usual monoclinic A phase, and the pure A phase, respectively. SEM micrographs of VO2 powders from the fined precursor demonstrated that the particle sizes of these fine powders were less than 2 μm. DSC curve of the VO2 obtained at 450 °C for 30 min from the fined precursor showed that there was an endothermic phase transition at 71 °C.

The computational capability of automatically determining the optimal control strategies for pressurized water reactor core maneuvering, in terms of an operating strategy generator (OSG), has been ...

As the increasing of vehicle, the problem of traffic jam is more prominent and the real-time traffic recognition systems come into being. Combine with the characteristic of vehicle distribution in congested roads, a real-time traffic recognition method was designed and implemented by visual space transformation and gridding. This method can recognize different traffic situations effectively and has a good accuracy. It can meet the real-time demands. Keywords—Intelligent Transportation, Real-time Traffic, Traffic Video 基于交通视频的路况分析方法的设计与实现 王秀 1 叶剑青 2 1) 福州大学数学与计算机科学学院,福州,福建,中国 2) 中国电信福建公司,福州,福建,中国 摘 要 随着出行车辆数量的增加,城市交通拥堵问题日益突出,路况分析系统应运而生。本文结合拥堵道路车辆分布特征,通 过对道路区域进行视觉空间转换网格化,设计并实现了一种基于交通视频的路况分析方法。通过对结果的分析表明,该方法可有效识 别道路拥堵情况,算法检测准确率高,识别速度快,满足实时性应用的需要。 关键词 智能交通系统,实时路况,交通视频 1.引言 随着经济和社会的快速发展,我国很多城市的市区面 积开始逐渐扩大,道路建设不断增多,出行车辆不断增加, 城市交通已经进入一个快速发展的阶段。但是,很多城市 在发展过程中普遍遇到了城市交通拥堵问题,解决城区交 通拥堵已成为许多城市迫在眉睫的重要任务[1]。 智能交通系统(ITS)的本质是通过传感技术、信号处 理技术、控制技术等现代信息技术与交通工程的综合应用, 以最大限度地发挥交通基础设施的潜力,并引导合理的交 通行业。通过应用 ITS,将传统的交通系统改造成一种信 息化、智能化、社会化的新型交通系统。实时路况分析系 统是智能交通系统的一个重要组成部分,通过实时路况分 析系统,出行者能够根据自己的意愿了解某条道路或某个 地点的畅通情况,从而选择最合适的出行行车路线。 基金项目:福州大学科技发展基金(2012-XY-20) 浮动车信息(FCD)采集技术是目前国际上 ITS 系统 中采集道路交通信息的主要技术手段,它利用定位技术、 无线通信技术和信息处理技术,实现对道路上行驶车辆的 瞬时速度、位置、路段旅行时间等交通数据的采集。经过 汇总、处理后这些信息生成反映实时道路拥堵情况的交通 信息。虽然 FCD 浮动车数据具有很强的连续性,可全天候 工作,提供的交通信息多样化,但要获得全路网的精确交 通信息就必须要有足够多的装有GPS接收设备的车辆驶行 在道路网络中。由于目前浮动车多以安装有 GPS 的营运车 辆为主。在交通高峰期,运营车辆司机凭借以往经验会在 高峰时段有意避开某些拥堵路段,导致此路段浮动数据量 较少而与实际路况拥堵情况不相符。而在非高峰时段营运 车辆经常会同时停靠在某些畅通路段(如等客,防止空载 行驶,节约成本),导致此类路段停止的浮动车数据量较多, 在地图路况展现上出现严重偏差。此外,所有的 FCD 浮动 车数据需要经过采集、处理、分析、展示等多个环节,最 International Conference on Future Computer and Communication Engineering (ICFCCE 2014) © 2014. The authors Published by Atlantis Press 189 终在地图上展现往往需要延时 5 至 7 分钟。 本文在对已有的视频处理技术及方法研究的基础上, 提出了一种基于交通视频的实时路况分析方法,在提高实 时路况准确性与及时性方面起到了较好的效果。该方法可 作为原有基于 FCD 浮动车数据采集的路况信息的有效补 充。 2.交通视频实时路况分析方法总体流程 人眼可以很容易地通过交通实时视频区别出路段是否 拥堵。通过对人眼识别道路拥堵的过程进行分析,我们发 现主要是由于拥堵路段车辆分布具有以下特点:一、拥堵 路道车辆较多;二、拥堵路道车辆间距较小。本文基于拥 堵路段的上述特点,对交通视频图像进行处理,并提出一 种基于视觉空间转换的网格化方法,实现道路特征提取与 实时路况分析。具体处理流程如下:确定道路区域,将交 通视频原始彩色图像做灰度化处理及平滑操作,然后在道 路区域中采用基于背景差分法进行运动物体提取,得到二 值化图像;通过对道路区域进行视觉空间网格化,并根据 上述拥堵路段车辆分布特点,对二值化图像进行分析,计 算路况特征指数与道路拥堵指数,以判断路段是否拥堵。

To systematically evaluate the prognostic value of lymphovascular invasion (LVI) in radical prostatectomy (RP) by a meta-analysis based on the published literature. To identify relevant studies, PubMed, Cochrane Library, and Web of Science database were searched from 1966 to May 2014. Finally, 25 studies (9503 patients) were included. LVI was found in 12.2% (1156/9503) of the RP specimens. LVI was found to be correlated with higher pathological tumor stages (greater than pT3 stage) (risk ratio [RR] 1.90, 95% confidence interval [CI] 1.73–2.08, P < 0.00001), higher Gleason scores (greater than GS = 7) (RR 1.30, 95% CI 1.23–1.38, P < 0.00001), positive pathological node (pN) status (RR 5.67, 95% CI 3.14–10.24, P < 0.00001), extracapsular extension (RR 1.72, 95% CI 1.46–2.02, P < 0.00001), and seminal vesicle involvement (RR 3.36, 95% CI 2.41–4.70, P < 0.00001). The pooled hazard ratio (HR) was statistically significant for Biochemical Recurrence-Free (BCR-free) probability (HR 2.05, 95% CI 1.64–2.56; Z = 6.30, P < 0.00001). Sensitivity analysis showed that the pooled HR and 95% CI were not significantly altered by the omission of any single study. Begg's Funnel plots showed no significant publication bias (P = 0.112). In conclusion, LVI exhibited a detrimental effect on the BCR-Free probability and clinicopathological features in RP specimens, and may prove to be an independent prognostic factor of BCR.