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Due to the combined pressures of energy shortage and environmental degradation, bio-liquid fuels have been widely studied as a green, environmentally friendly, renewable petroleum alternative. This article summarizes the various technologies of three generations of biomass feedstocks (especially the second-generation, biomass lignin, and the third-generation, algae raw materials) used to convert liquid fuels (bioethanol, biodiesel, and bio-jet fuel) and analyzes their advantages and disadvantages. In addition, this article details the latest research progress in biomass liquid fuel production, summarizes the list of raw materials, products and conversion processes, and provides personal opinions on its future development. The aim is to provide a theoretical basis and reference for the optimization of existing technology and future research and development of biomass liquid fuels.

OBJECTIVE: To assess impact of personal protective equipment (PPE) on healthcare providers (HCPs) in caring for COVID-19 patients. METHODS: A cross-sectional survey was conducted over 50 hospitals in China. Descriptive analyses and Chi-square tests were performed on the collected data. RESULTS: All 104 frontline HCPs report negative impacts of PPE on their clinical performance, 97% of them experienced discomfort and injuries caused by wearing PPE for long hours. Frontline HCPs provided suggestions to alleviate the negative impacts and to enhance communication between healthcare staff and patients. Two hundred eighty two non-frontline HCPs also revealed similar problems; however, we recorded a few discrepancies between answers given by frontline and non-frontline HCPs. CONCLUSIONS: Wearing PPE for long hours degrades health performance. Measures were suggested to improve the design of PPE for protecting HCPs and enhancing their services to COVID patients.

Idiopathic pulmonary fibrosis (IPF) is an agnogenic, rare, and lethal disease, with high mortality and poor prognosis and a median survival time as short as 3 to 5 years after diagnosis. No effective therapeutic drugs are still not available not only in clinical practice, but also in preclinical phases. To better and deeper understand pulmonary fibrosis will provide more effective strategies for therapy. Mounting evidence suggests that noncoding RNAs (ncRNAs) and their interactions may contribute to lung fibrosis; however, the mechanisms underlying their roles are largely unknown. In this review, we systematically summarized the recent advances regarding the crucial roles of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) and crosstalk among them in the development of IPF. The perspective for related genes was well highlighted. In summary, ncRNA and their interactions play a key regulatory part in the progression of IPF and are bound to provide us with new diagnostic and therapeutic targets.

Background Although video-assisted thoracoscopic surgery (VATS) is increasingly used, the optimal analgesia strategy is still unknown. We explore the efficacy and safety of preemptive ultrasound-guided paravertebral block (PVB) combined with parecoxib during VATS. Methods Seventy-four patients were divided into two groups. PVBs were performed before anesthesia induction under real-time ultrasound guidance. Visual analog scale (VAS) score with coughing at 48 h after surgery, postoperative sufentanil consumption and level of sedation (LOS) at 1, 4, 8, 12, 24, and 48 h postoperatively, intraoperative hemodynamics, satisfaction scores of patients and surgeons, remedial measures, time to chest tube removed and mobilization, adverse effects and hospital stay length were recorded. We also recorded inflammatory markers, respiratory function and the prevalence of chronic pain after surgery. Results VAS scores at rest and with coughing during the first 24 h after surgery were significantly lower in the P group (P

Background and aim: It is of the utmost importance for the specific diagnosis and effective therapy of hepatocellular carcinoma (HCC). Abnormality of oncogenic Wingless-type MMTV integration site family member 3a (Wnt3a) has been associated with progression of HCC. In this study, we aimed to evaluate Wnt3a as a novel biomarker and target for HCC. Methods: Circulating Wnt3a levels were quantitatively detected in a cohort of chronic liver diseases by an enzyme-linked immune-absorbent assay (ELISA). Hepatic Wnt3a expression in HCC and para-cancerous tissues was analyzed by immunohistochemistry. Prognostic value of Wnt3a for HCC was discovered in the cohort from the Cancer Genome Atlas (TCGA). Dynamic alterations of Wnt3a levels were detected in the hepatocarcinogenesis model induced by 2-acetylaminofluorene. Effects of Wnt3a on biological behaviors were evaluated in vitro and in vivo based on Crispr/Cas9. Results: Up-regulated Wnt3a levels were observed in serum of HCC patients with high specificity and sensitivity for HCC diagnosis. Combination of Wnt3a and AFP could improve sensitivity to 93.9% in serological detection. In addition, Wnt3a expression in HCC tissues was significantly higher than that in para-cancerous tissues. The cohort of TCGA demonstrated that high Wnt3a expression led to a poor survival of HCC patients, especially in cases at advanced stages. Furthermore, the hepatocarcinogenesis model showed that Wnt3a dynamically increased in the development of HCC. Functionally, silencing Wnt3a by Crispr/Cas9 suppressed the proliferation, colony formation, induced cell cycle arrest of HCC cells by de-activating Wnt/β-catenin pathway in vitro, and inhibited xenograft tumor growth in vivo. Conclusions: Oncogenic Wnt3a could be considered as a candidate biomarker and novel target for HCC.

The university has always been the main front of political and ideological construction. The ideological and political form of the young faculty group consisting of important teachers is particularly important. Under the background of China's current reforms entering the deep water area and tackling the hardship period, it is of great significance to effectively consolidate the ideological consensus, political identity, and political identity of young teachers in colleges and universities. On this basis, this study combines the methods of qualitative analysis and quantitative analysis, using binary logistic regression model, scientifically analyzes and accurately identifies the factors that influence the identification of ideological and political education systems for young teachers in colleges and universities. On this basis, it proposes to recognize the institutional performance release system. The institutionalized countermeasure system strengthens institutional identity through institutional advantages and respects the recognition of a solid system with political beliefs.

Objectives A novel coronavirus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is causing the worldwide coronavirus disease 2019 (COVID-19) outbreak with high mortality. A unique finding among COVID-19 patients was a decline of eosinophil levels (eosinopenia). However, results from previous studies on the relationship between eosinopenia and disease severity were inconsistent. The objective of this study is to determine the relationship between eosinopenia and COVID-19 mortality as well as the clinical conditions that could potentially lead to mortality. Methods One hundred ninety patients diagnosed as moderate, severe, or critical COVID-19 at hospital admission were enrolled. Data collected from patients’ medical records on the second day after hospital admission included medical histories, clinical symptoms, chest images of computed tomography (CT), laboratory examinations, and outcomes. Results Eosinophil levels were significantly lower in patients with critical disease, when compared to those with moderate and severe diseases. After controlled for confounding factors, ie, age, gender, hypertension, coronary heart disease, diabetes, and chronic lung disease, a progressive decline of eosinophil levels was independently associated with mortality. Moreover, eosinophil levels significantly and positively correlated with platelet and D-dimer levels but significantly and inversely correlated with serum levels of urea, creatinine, aspartate aminotransferase, lactate dehydrogenase, and creatine kinase. Conclusions Eosinopenia, if progressively worsening, indicates that COVID-19 patients may progress to critical disease and have a significantly higher chance of mortality. Additionally, eosinopenia correlates with biomarkers of coagulation disorder and those of tissue damage in kidney, liver, and other tissues.

Acute respiratory distress syndrome (ARDS) induced by sepsis contributes remarkably to the high mortality rate observed in intensive care units, largely due to a lack of effective drug therapies. Histone deacetylase 6 (HDAC6) is a class-IIb deacetylase that modulates non-nuclear protein functions via deacetylation and ubiquitination. Importantly, HDAC6 has been shown to exert anti-cancer, anti-neurodegeneration, and immunological effects, and several HDAC6 inhibitors have now entered clinical trials. It has also been recently shown to modulate inflammation, and HDAC6 inhibition has been demonstrated to markedly suppress experimental sepsis. The present review summarizes the role of HDAC6 in sepsis-induced inflammation and endothelial barrier dysfunction in recent years. It is proposed that HDAC6 inhibition predominantly ameliorates sepsis-induced ARDS by directly attenuating inflammation, which modulates the innate and adaptive immunity, transcription of pro-inflammatory genes, and protects endothelial barrier function. HDAC6 inhibition protects against sepsis-induced ARDS, thereby making HDAC6 a promising therapeutic target. However, HDAC inhibition may be associated with adverse effects on the embryo sac and oocyte, necessitating further studies.

The current outbreak of Coronavirus Disease 2019 (COVID-19) has raised great concern worldwide, but its impact on transplant recipients is unknown. We report here the clinical features and therapeutic course of the first reported renal transplant recipient with confirmed COVID-19 pneumonia. This is a 52-year-old man who received kidney transplantation 12 years ago. His overall clinical characteristics (symptoms, laboratory examinations, and chest CT) were similar to those of non-transplanted COVID-19 patients. Following a treatment regimen consisting of reduced immunosuppressant use and low dose methylprednisolone-based therapy, the COVID-19 pneumonia in this long-term immunosuppressive patient was successfully recovered. This effectively treated case has reference value for the future treatment of other transplant patients with COVID-19 pneumonia.

Wenjie Zheng,1,2,* Junling Yang,2,* Zhizhen Dong,3,* Li Wang,1 Miao Fang,1 Wei Wu,2 Dengfu Yao,1,2 Min Yao1 1Medical School of Nantong University, Nantong 226001, Jiangsu, China; 2Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China; 3Department of Diagnostics, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China *These authors contributed equally to this work Purpose: High mobility group box 3 (HMGB3) is associated with hepatocytes malignant transformation by our previous work. We continued to investigate the diagnostic and prognostic values of HMGB3 for hepatocellular carcinoma (HCC). Patients and methods: Circulating HMGB3 levels were quantitatively detected in a cohort of 225 patients with chronic liver diseases by ELISA and compared with alpha-fetoprotein by the receiver operating characteristic curve. HMGB3 expression in tissues of 170 HCC was detected by tissue microarray and immunohistochemistry. Relationship between HMGB3 level and HCC prognosis was evaluated by the Kaplan–Meier curves and Cox regression model. Results: The incidence of serum HMGB3 >2.0 ng/mL was 75.6% in HCC (96/127), 20.8% in liver cirrhosis (10/48), 16.0% in chronic hepatitis (8/50), and none in healthy controls (0/49). Significant difference (P30.6% in their paracancerous tissues (52/170). HMGB3 expression was closely related to tumor size, TNM stage, poor survival, and high recurrence, suggesting an independent prognosis factor for HCC. Conclusion: HMGB3 with aberrant expression could be a novel diagnostic and prognostic marker for HCC. Keywords: hepatocellular carcinoma, HMGB3, diagnosis, prognosis, biomarker

Panax ginseng is a natural medicine that has been used globally for a long time. Moreover, several studies have reported the effective activity of ginseng in treating malignancies. Various agents containing ginseng were widely used as an antitumor treatment nowadays. Lung cancer is the most common fatal cancer in China, and lung adenocarcinoma is the most common histological type of non-small cell lung cancer (NSCLC). What’s worse, many patients may have a failed response to conventional therapy including chemotherapy, radiotherapy, or molecule-targeted therapy due to drug resistance. Apoptosis is a highly ordered cellular suicidal process that plays an essential role in maintaining normal homeostasis. The pharmacological mechanism of many antineoplastic drugs involves triggering of apoptotic process. In several recent studies, ginsenosides are regarded as major active components of ginseng that have the potential to control lung cancer. Most of these results have proved that ginsenosides induce apoptosis in lung cancer cells through many different signaling pathways such as PI3K/Akt, NF-[Formula: see text]B, EGFR, and so on. This study is aimed at reviewing the signaling pathways that underlie ginsenosides-triggered apoptotic process and encourage further studies to target promising agents against lung cancer treatment.

Fatigue is a common symptom in patients with ankylosing spondylitis (AS). However, fatigue of AS patients has not been well elucidated in China. This study aimed to evaluate the predictors of fatigue and the effects of fatigue on health-related quality of life among patients with AS.A total of 150 AS patients were involved in the study. A series of questionnaires included the following: Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Metrology Index (BASMI), Bath Ankylosing Spondylitis Functional Index (BASFI), the 10-cm Visual Analog Scale (VAS), the Self-Rating Anxiety Scale (SAS), the Self-Rating Depression Scale (SDS), the Pittsburgh Sleep Quality Index (PSQI), the Health Assessment Questionnaire-Disability Index (HAQ-DI), the Short Form 36 Health Survey (SF-36), and the Fatigue Severity Scale (FSS). Independent samples t test, Mann-Whitney U test, chi-square analysis, Pearson/Spearman correlation, and binary logistic regression were used to analyze the data.The results demonstrated that 48.7% individuals with AS suffered from fatigue. Binary logistic regression indicated that waist-to-hip ratio, BASDAI, and sleep disturbance were independent predictors of fatigue in AS patients. Meanwhile, severe fatigue led to lower quality of life.These findings suggested that medical personnel should pay more attention to AS patients with fatigue and take effective measures to relieve fatigue. Key Points • Incidence of fatigue in AS patients is 48.7% according to this cross-sectional study. • The occurrence of fatigue was associated with higher WHR, higher BASDAI, and sleep disturbance. • We also found that the occurrence of fatigue significantly reduced the quality of life in AS patients both physically and psychologically.

// Wenjie Zheng 1, * , Min Yao 2, * , Qi Qian 3, * , Wenli Sai 1 , Liwei Qiu 1 , Junling Yang 1 , Wei Wu 1 , Zhizhen Dong 1, 4 and Dengfu Yao 1 1 Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China 2 Department of Immunology, Medical School of Nantong University, Nantong 226001, Jiangsu Province, China 3 Department of Oncology, Yancheng 1 st People’s Hospital, Yancheng 224005, Jiangsu Province, China 4 Department of Diagnostics, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China * These authors have contributed equally to this work Correspondence to: Dengfu Yao, email: yaodf@ahnmc.com Zhizhen Dong, email: dongzz@ahnmc.com Keywords: hepatocellular carcinoma, secretory clusterin, prognosis, tumor stage, tumor growth Received: September 20, 2016 Accepted: November 18, 2016 Published: November 29, 2016 ABSTRACT Secretory clusterin (sCLU) is associated with hepatocellular carcinoma (HCC) progression by contributing to angiogenesis, chemoresistance, cell survival, and metastasis. However, the sCLU expression at early stage of HCC progression remains to be clarified. In this study, the alteration of sCLU oncogenicity was firstly evaluated in HCC- and their para-cancerous- tissues. The incidence of sCLU expression in HCC was significantly higher than that in their non-tumorous tissues at message RNA (mRNA) or protein level, gradually increasing with tumor-node-metastasis (TNM) staging. Abnormal sCLU expression was associated with the poor differentiation, TNM stage, and considered as an independent prognostic factor for HCC patients. Furthermore, silencing sCLU gene transcription inhibited the colony formation and proliferation of HCC cells, with decreasing phosphorylation level of AKT and GSK-3β in HCCLM3 cells in vitro and significantly suppressed the HCC xenograft growth in vivo, suggesting that sCLU with oncogenicity should be not only an early indicator but also novel potential molecular-targeted therapy for HCC.

China has entered a critical period of reform and development and contemporary college students will become an important driving force. Under such circumstances, it is of great significance to consolidate their political institutional identity for maintaining political stability and promoting social progress. Based on the survey data of colleges and universities in central China, this paper, using ordinal logistic regression analysis model (ologit model), scientifically analyzes and accurately identifies the factors influencing the political institutional identity of college students. The empirical results show that, as far as the institution itself is concerned, its fairness, representation and performance have a positive and systematic on institutional identity. In terms of external factors, the cultivation of individual values has a significant positive impact on institutional identity, while multi-culture will lead to the deviation in institutional identity. On this basis, this paper puts forward some suggestions to promote the political institutional identity of college students from the aspects of institutional arrangement, ideological education and social environment.

Ethnopharmacological relevance Many bioactive constituents of Chinese herbal medicines have poor oral bioavailability. Besides oral administration, herbal medicines in China are also prepared for parenteral administration. Unlike for intravenous route, little is known about the intramuscular pharmacokinetics of herbal compounds. To facilitate rational use of herbal medicine, it is important to better understand such intramuscular pharmacokinetics. Aim of the study Bioactive constituents of XueShuanTong (a lyophilized extract of Panax notoginseng roots, extensively used in treatment of ischemic heart and cerebrovascular diseases) predominantly comprise ginsenosides Rb1 and Rd of 20(S)-protopanaxadiol-type and ginsenosides Rg1, and Re, and notoginsenoside R1 of 20(S)-protopanaxatriol-type; these saponins are poorly absorbed from the gastrointestinal tract. This study aimed to compare intramuscular and intravenous pharmacokinetics of these ginsenosides after dosing XueShuanTong. Methods Pharmacokinetics of ginsenosides was assessed in human volunteers receiving an intramuscular injection or 1.5-h intravenous infusion of XueShuanTong, both at 150 mg/person, and the plasma and urine samples were analyzed by liquid chromatography/mass spectrometry. Results Like after intravenous administration, the unchanged saponins were the major circulating forms after intramuscular administration, while their metabolites were poorly detected. These ginsenosides exhibited intramuscular bioavailability of 100%–112%, relative to the respective intravenous data. Similar to that after intravenous infusion, the 20(S)-protopanaxadiol-type ginsenosides after the intramuscular injection exhibited notably longer terminal half-lives (46–106 h) than the 20(S)-protopanaxatriol-type ginsenosides (1.1–1.4 h). Conclusions Intramuscular route might be an effective alternative to intravenous route for XueShuanTong, from the pharmacokinetic perspective.

The mechanism of local inflammation and systemic injury in chronic periodontitis is complicated, in which and exosomes play an important role. In our study, we found that T helper cell 17 (Th17)/regulatory T cell (Treg) balance is destabilized in the peripheral blood of patients with periodontitis, with upregulated Th17 or downregulated Treg, respectively. Porphyromonas gingivalis lipopolysaccharide (LPS) was used to simulate the inflammatory microenvironment of chronic periodontitis. The exosomes were extracted from periodontal ligament stem cells (PDLSCs) in LPS-induced periodontitis environment, which inversely effected on CD4+ T cells under normal and inflammatory conditions. Furthermore, compared with exosomes from normal PDLSCs, lower expression of microRNA-155-5p (miR-155-5p) and higher expression of Sirtuin-1 (SIRT1) were observed in exosomes from LPS-stimulated PDLSCs. Exosomes from PDLSCs alleviated inflammatory microenvironment through Th17/Treg/miR-155-5p/SIRT1 regulatory network. This study aimed to find the "switching" factors that affected the further deterioration of periodontitis to maximally control the multiple downstream damage signal factors to further understand periodontitis and find new targets for its treatment.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease involving multiple organs and systems. Mesenchymal stem cells (MSCs) from SLE patients have demonstrated defects such as impaired growth, senescence phenotype and immunomodulatory functions. Some studies have suggested the close connection between inflammation microenvironment and cellular senescence. In the current study, we detected cytokines levels in bone marrow supernatant by the quantitative proteomics analysis, and found the expression of HMGB1 was remarkably increased in bone marrow from SLE patients. Senescence associated-β-galactosidase (SA-β-gal) staining, F-actin staining and flow cytometry were used to detect the senescence of cells. After stimulation of HMGB1 in normal MSCs, the ratio of SA-β-gal positive in BM-MSCs was increased, the organization of cytoskeleton was disordered, and TLR4-NF-κB signaling was activated. Finally, Ethyl pyruvate (EP) (40 mg/kg and 100 mg/kg, three times a week), a high security HMGB1 inhibitor, was injected intraperitoneally to treat MRL/lpr mice for 8 weeks. We demonstrated that EP alleviated the clinical aspects of lupus nephritis and prolonged survival of MRL/lpr mice. In the meantime, EP reversed the senescent phenotype of BM-MSCs from MRL/lpr mice. HMGB1 could be a promising target in SLE patients, and might be one of the reasons of recurrence after MSCs transplantation.

Backgroud: As the development of urbanization in China, the morbidity of allergic diseases rises up significantly even in children. But the mechanism of the protection from microorganisms in rural environment needs still to be elucidated in detail. Methods: Pregnant women living in farming or non-farming environment were prospectively recruited and questionnaires were completed before delivery. Endotoxin and glucans in dust from living room of pregnant mothers were collected and analyzed. During delivery, cord blood mononuclear cells were isolated and cultured with stimulation of PHA, LPS or PPG. CD4+CD25+FOXP3+T cells and specific cytokines of Th and Tregs were tested with flow cytometry, Tregs specific genes were detected with RT-PCR, suppressive capacity of Tregs was tested by culturing with effector cells in vitro, and TLR2/4 gene polymorphism was detected at last. Results: Higher endotoxin content in living room of mothers was shown in farming environment comparing with non-farming in Jilin province of China. The tendency of increased Th1 cell polarity as well as decreased Th2 cell polarity on TLR2/4 response pathway in newborn with farming mother had been shown. The quantity of Tregs, gene expression of FOXP3 and GITR, and suppressive effect of Tregs increased on TLR2/4 response pathway in farming group. The polymorphism TLR2-15607 and TLR2-16934 in newborn could affect FOXP3 expression, IFN-γ and IL-13 production on TRL2/4 response pathway in different way, depending on different maternal microbial environment. Conclusions: Maternal living in farming environment with microbial overloading reduced the susceptibility of offspring to allergic diseases.

This study aimed to investigate the effects of tumor necrosis factor-α (TNF-α) on systemic lupus erythematosus (SLE). The animal model of MRL/MpJ-Faslpr mice (MRL/lpr; lupus-prone mice) showed depression-like behaviors based on tail suspension, sucrose preference, and open field tests. Brain microglia were significantly activated with obvious increases in proinflammatory cytokines. In addition, in vitro experiments showed that TNF-α activated microglia by upregulating the NF-κB signaling pathway and proinflammatory cytokines. PDTC, a specific NF-κB inhibitor, effectively reduced TNF-α-mediated inflammatory signaling in microglia. These results suggest that TNF-α-induced microglial activation has a major role in neuroinflammation of SLE with depression.

Background Systemic lupus erythematosus (SLE) is a complex autoimmune disease accompanied by damage to a variety of tissue injuries, such as joints, kidney, and the peripheral and central nervous systems (CNS).1 The diffuse CNS lupus manifests with a diverse array of neuropsychiatric symptoms that range from headaches, anxiety, depression, to cognitive impairment and, in rare cases, psychosis.2 Additionally, up to 24% of SLE patients will display depression.3 Previus studies have suggested microglia, as critical mediators of depression in SLE. Objectives To date, the pathophysiology of most depression symptoms in SLE has not been well determined. We focused our attention on the potential role of microglia in neuroinflammation in SLE patients. Methods Cerebrospinal fluid was collected from 3 healthy people and 3 SLE patients. According to the hospital anxiety and depression scale (HADS), we investigate the depression of SLE patients. The cytokines were screened using a RayBio Human Cytokine Antibody Array in cerebrospinal fluid samples by analysing a variety of inflammatory cytokines such as IL-6, Leptin and TNF-α. Cerebrospinal fluid of SLE patients and normal people were tested by ELISA for TNF-α. The depression status of MRL/lpr (C3MRL-Faslpr/J) mice and Balb/c mice was determined by tail suspension test, open-field test and sucrose preference test. Immunofluorescence and Western blot was utilised to detect the activation of microglial cells in brain tissue. Microglia cells were stimulated by TNF-α, Western blot showed the expression of CD68 and activated NF-κB. The concentrations of IL-6 and IL-1β in the cell supernatants were measured by ELISA. After using of NF-КB signalling pathway inhibitor PDTC, the activation of microglia stimulated by TNF-α was determined by immunofluorescence, quantitative PCR, Western blot analysis and ELISA. Results The results showed that the level of TNF-α in cerebrospinal fluid of patients with lupus was higher than normal people. At 14 weeks, MRL/lpr mice appear depression by tail suspension test, open-field test and sucrose preference test, MRL/lpr mice had more reactive microglia in the cortex when compared to Balb/c. After microglial cell were stimulated by TNF-α, microglias were active and effectively release IL-6, IL-1β and iNOS. Moreover, the expression of CD68 and activated NF-κB signalling pathway were also higher significantly. However, the use of NF-κB signalling pathway inhibitor PDTC reverse the TNF-α induced microglial activation. Conclusions The study showed that the different level of inflammatory cytokines of cerebrospinal fluid of SLE patients. Our results highlight the potential role of microglia in neuroinflammation in SLE patients with depression. References [1] Bialas AR, et al. Microglia-dependent synapse loss in type I interferon-mediated lupus. Nature2017. [2] McHugh J. Systemic lupus erythematosus: IFN drives synapse loss via microglia. Nat Rev Rheumatol2017;13(8):449. [3] Zhang L, et al. Prevalence of depression and anxiety in systemic lupus erythematosus: a systematic review and meta-analysis. BMC Psychiatry2017;17(1):70. Acknowledgements This work was supported by grants from The Natural Science Foundation of China under Grant (81401124)and The Natural Science Foundation of China under Grant (8167060931). Disclosure of Interest None declared

Background Systemic lupus erythematosus (SLE is a chronic autoimmune disease that systemically affects several important organs[.1 Lupus nephritis (LN is one of the most severe complications of SLE[.2 Exosomes are important mediators of biological information and play a part in the occurrence and development of various diseases including LN[.3 Objectives The aim of study was to find whether exosomes participate in the pathogenesis of lupus nephritis. Methods We studied 10 patients with SLE but no LN,10 patients with LN and 10 healthy people which are in line with the SLE classification criteria of American College of Rheumatology diagnostic (ACR) in 1997 and the LN pathological classification of ISN and RPS in 2003. Exosomes were isolated from the serum by ultracentrifugation and confirmed by transmission electron microscope and western blot. The internalisation of exosomes was detected by immunofluorescence Then exosomes were injected into MRL/lpr mouse via the tail vein and co-cultured with mesangial cells. Flow cytometry was used to detect the alteration of cell cycle. The cell proliferation was determined by CCK-8 assay. The inflammatory cytokines (TNF-α, IL-6) and collagen I level in medium supernatant by ELISA, signal pathway by immunoblotting. Additionally, High-throughput sequencing was used to detect the expression of miRNAs in exosomes. Results The proteinuria and the percent of kidney crescent formation index of LN group was significantly high than oher three groups. Exosomes can be absorbed by mesangial cells quickly. The secrection of inflammatory cytokines and collagen Iof LN group were higher than NLN and control group(p Conclusions LN exosomes can enhance the proliferation and secrection of mesangial cells in which PI3K/AKT pathway is actived. This tip us exosomes may involve in the pathogenesis of LN. References [1] Shen B, Tan W, Feng G, He Y, Liu J, Chen W, Huang X, Da Z, Xu X, Liu H, Gu Z. The correlations of disease activity, socioeconomic status, quality of life, and depression/anxiety in Chinese patients with systemic lupus erythematosus. Clinical & developmental immunology2013;270878. [2] Chafin CB, Reilly CM. MicroRNAs implicated in the immunopathogenesis of lupus nephritis. Clinical & developmental immunology2013;430239. [3] Abels ER, Breakefield XO. Introduction to Extracellular Vesicles: Biogenesis, RNA Cargo Selection, Content, Release, and Uptake. Cellular and molecular neurobiology2016. Acknowledgements The Natural Science Foundation of China under Grant (81202368), The Natural Science Foundation of China under Grant (81471603) Disclosure of Interest None declared

Background Mesenchymal stem cells (MSCs) exert chondroprotective effects in clinical models of osteoarthritis (OA), but the exact mechanisms were still unclear. Exosomes that serve as carriers of genetic information have been implicated in many diseases and are known to participate in many physiological processes. Objectives Here, we investigate the therapeutic potential of exosomes from human bone marrow MSCs in alleviating OA and explore the mechanism. Methods Exosomes were harvested from conditioned culture media of BM-MSCs by a sequential centrifugation process. The anterior cruciate ligament transection and destabilisation of the medial meniscus (DMM) surgery were performed on the knee joints of SD female rat as an OA model. After four weeks, the animals were followed by intra-articular injection of either BM-MSCs or their exosomes every week for four weeks. Cartilage destruction, matrix degradation and subchondral bone changes were evaluated with histological staining and micro-CT at the post-surgery 8 weeks. Primary human chondrocytes treated with IL-1β were used as an in vitro model to evaluate the effects of exosomes for 24 hours. Results We found that intra-articular injection of BM-MSCs and BM-MSCs derived exosomes improve cartilage destruction and subchondral bone remodelling in ACLT+DMM model. BM-MSCs and exosomes equally protected rat from joint damage. These exosomes maintained the chondrocyte matrix by increasing collagen type II synthesis and decreasing ADAMTS5, MMP13 and Col II expression in the presence of IL-1β in vitro. In addition, BM-MSCs derived exosomes were also shown to protect chondrocytes from apoptosis and senescence. Conclusions The exosomes from BM-MSCs exert a beneficial therapeutic effect on OA by not only repairing the degenerative cartilage, but also improving subchondral bone remodelling, which in turn provides a new target for OA drug and drug-delivery system development. References [1] Trounson A, McDonald C. Stem Cell Therapies in Clinical Trials: Progress and Challenges. Cell stem cell2015;17:11–22. [2] Stoorvogel W, Kleijmeer MJ, Geuze HJ, Raposo G. The biogenesis and functions of exosomes. Traffic2002;3:321–30. [3] Lai RC, Yeo RW, Lim SK. Mesenchymal stem cell exosomes. Seminars in cell & developmental biology2015;40:82–8. [4] Zhang S, Chu WC, Lai RC, Lim SK, Hui JH, Toh WS. Exosomes derived from human embryonic mesenchymal stem cells promote osteochondral regeneration. Osteoarthritis and cartilage2016;24:2135–40. [5] Wang Y, Yu D, Liu Z, et al. Exosomes from embryonic mesenchymal stem cells alleviate osteoarthritis through balancing synthesis and degradation of cartilage extracellular matrix. Stem cell research & therapy2017;8:189. Acknowledgements No. Disclosure of Interest None declared

The amyloid hypothesis has been the main theory to explain the etiology of Alzheimer’s disease (AD) and provided potentially preventive and therapeutic targets. Although Aβ-immunotherapy holds promise for AD, its vascular complications reduce the efficacy and safety. We produced an adeno-associated virus vector encoding Aβ-specific catalytic antibody, rAAV9-IgV L 5D3, and evaluated the prophylactic and therapeutic efficacy and safety of rAAV9-IgV L 5D3 brain delivery in an AD mouse model. One single injection of rAAV9-IgV L 5D3 into the right ventricle achieved widespread, high expression of IgV L 5D3 in the right hippocampus and cerebrospinal fluid but less expression in the left hemisphere. The prophylactic and therapeutic application of rAAV9-IgV L 5D3 reduced Aβ load in the right hippocampus. The therapeutic application improved long-term but not short-term memory on the Morris water maze without increasing cerebral amyloid angiopathy, microhemorrhage, and inflammation. Brain-targeted gene delivery of Aβ-specific catalytic antibody can be a safer and more effective approach for AD prevention and treatment than conventional anti-Aβ antibodies.

The objective of this study was to assess the clinical and histopathological relationship between pulmonary fibrosis and type 1 diabetes. We examined clinical pulmonary function parameters and transbronchial lung biopsies to assess associated histopathological changes in 12 type 1 diabetic patients presenting with dyspnea. Lung CT images pulmonary function tests from 12 diabetic patients without dyspnea and from 12 matched normal subjects served as controls. A similar histopathological analysis, including cytokine levels and pro-fibrotic markers, was performed on lung tissues in mice after the induction of experimental diabetes in an attempt to strengthen the link between diabetes and pulmonary fibrosis. Pulmonary function parameters (FVC, FEV1, TLC, and DLco/VA) were significantly reduced in diabetic patients with dyspnea and without dyspnea, compared to controls. Both patient groups also had increased lung CT scores and symptoms compared to normal controls, though the greatest increases were in the diabetic patients with dyspnea. Chronic hyperglycemia induced in mice led to histopathological changes in the lungs that were similar to those found in the human diabetic subjects and included alveoli compression by hyperplastic interstitium infiltrated with inflammatory cells and fibrotic in nature. Two inflammatory related genes, TNF-α and PAI-1, and two fibrosis-related genes, CTGF and fibronectin, demonstrated increased mRNA and protein expression in diabetic mouse lungs. In conclusion, there were significant clinical and histopathological correlations between pulmonary fibrosis and the presence of type 1 diabetes. Diabetes was clinically associated with pulmonary fibrosis and dysfunction in humans, and diabetes induction led to a similar pulmonary fibrosis in an experimental model. These clinical and non-clinical data suggest that diabetes is an independent risk factor for pulmonary fibrosis.

Accumulation of amyloid beta-peptide (Aβ) in the brain is hypothesized to be a causal event leading to dementia in Alzheimer's disease (AD). Aβ vaccination removes Aβ deposits from the brain. Aβ immunotherapy, however, may cause T cell- and/or Fc-receptor-mediated brain inflammation and relocate parenchymal Aβ deposits to blood vessels leading to cerebral hemorrhages. Because catalytic antibodies do not form stable immune complexes and Aβ fragments produced by catalytic antibodies are less likely to form aggregates, Aβ-specific catalytic antibodies may have safer therapeutic profiles than reversibly-binding anti-Aβ antibodies. Additionally, catalytic antibodies may remove Aβ more efficiently than binding antibodies because a single catalytic antibody can hydrolyze thousands of Aβ molecules. We previously isolated Aβ-specific catalytic antibody, IgVL5D3, with strong Aβ-hydrolyzing activity. Here, we evaluated the prophylactic and therapeutic efficacy of brain-targeted IgVL5D3 gene delivery via recombinant adeno-associated virus serotype 9 (rAAV9) in an AD mouse model. One single injection of rAAV9-IgVL5D3 into the right ventricle of AD model mice yielded widespread, high expression of IgVL5D3 in the unilateral hemisphere. IgVL5D3 expression was readily detectable in the contralateral hemisphere but to a much lesser extent. IgVL5D3 expression was also confirmed in the cerebrospinal fluid. Prophylactic and therapeutic injection of rAAV9-IgVL5D3 reduced Aβ load in the ipsilateral hippocampus of AD model mice. No evidence of hemorrhages, increased vascular amyloid deposits, increased proinflammatory cytokines, or infiltrating T-cells in the brains was found in the experimental animals. AAV9-mediated anti-Aβ catalytic antibody brain delivery can be prophylactic and therapeutic options for AD.

Diabetic cardiomyopathy (DCM) is a common and severe complication of diabetes and results in high mortality. It is therefore imperative to develop novel therapeutics for the prevention or inhibition of the progression of DCM. Oxidative stress is a key mechanism by which diabetes induces DCM. Hence, targeting of oxidative stress-related processes in DCM could be a promising therapeutic strategy. To date, a number of studies have shown beneficial effects of several natural products on the attenuation of DCM via an antioxidative mechanism of action. The aim of the present review is to provide a comprehensive and concise overview of the previously reported antioxidant natural products in the inhibition of DCM progression. Clinical trials of the antioxidative natural products in the management of DCM are included. In addition, discussion and perspectives are further provided in the present review.

To interfere with the activation of nuclear factor-κB (NF-κB) with metformin and explore its effect in reversing multidrug resistance (MDR) of hepatocellular carcinoma (HCC) cells.Expression of P-glycoprotein (P-gp) and NF-κB in human HepG2 or HepG2/adriamycin (ADM) cells treated with pCMV-NF-κB-small interference RNA (siRNA) with or without metformin, was analyzed by Western blot or fluorescence quantitative PCR. Cell viability was tested by CCK-8 assay. Cell cycle and apoptosis were measured by flow cytometry and Annexin-V-PE/7-AnnexinV apoptosis detection double staining assay, respectively.P-gp overexpression in HepG2 and HepG2/ADM cells was closely related to mdr1 mRNA (3.310 ± 0.154) and NF-κB mRNA (2.580 ± 0.040) expression. NF-κB gene transcription was inhibited by specific siRNA with significant down-regulation of P-gp and enhanced HCC cell chemosensitivity to doxorubicin. After pretreatment with metformin, HepG2/ADM cells were sensitized to doxorubicin and P-gp was decreased through the NF-κB signaling pathway. The synergistic effect of metformin and NF-κB siRNA were found in HepG2/ADM cells with regard to proliferation inhibition, cell cycle arrest and inducing cell apoptosis.Metformin via silencing NF-κB signaling could effectively reverse MDR of HCC cells by down-regulating MDR1/P-gp expression.

Diabetic complications affect many organs in diabetic patients. Emerging evidence indicates that diabetes can increase the risk of pulmonary dysfunction. Early epidemiological studies from different populations on whether diabetes was an independent risk for pulmonary dysfunction were inconclusive. Recent epidemiological studies and systematic reviews clearly indicate that diabetes is an independent risk factor for pulmonary dysfunction. Given that pulmonary fibrosis is an important predictor of mortality in people with this chronic disease, whether diabetes directly causes pulmonary fibrosis is an important unresolved clinical question. This review combines recent epidemiological data with findings from basic research to indicate that diabetes induces pulmonary fibrosis. We then discuss the possible underlying mechanisms for the histological and biochemical pathology. At the end of this review, we emphasize that diabetic pulmonary fibrosis as a potential diabetic complication warrants more attention.

The injuries of the peripheral nerve are the results of trauma, disease, and surgical procedures that require section of peripheral nerves to gain access to the surgical site. Unlike elements of the central nervous system, peripheral nerves can regenerate when damaged. Recent studies provide evidence that intercellular adhesion molecule-1 (ICAM-1) is involved not only in inflammation, but also in cell recruitment during Wallerian degeneration after peripheral nerve injury. In our studies, two different injury models (crush and transect) for peripheral nerve regeneration were used. We investigated the dynamic changes of ICAM-1 expression in peripheral nervous system, including sciatic nerves and the dorsal root ganglia (DRG) following sciatic nerve injury. Double labeling demonstrated the presence of ICAM-1 within both Schwann cells and nerve blood vein endothelia cells in sciatic nerve after injury. In ipsilateral DRG, a few ICAM-1 signals were found in satellite cells, and ICAM-1 staining was mainly distributed in neuron. The results implied that ICAM-1 might be correlated with the function of Schwann cells about myelinogenesis and nerve regeneration.

Spy1, as a member of the Speedy/RINGO family and a novel activator of cyclin-dependent kinases, was shown to promote cell cycle progression and cell survival in response to DNA damage. While its expression and roles in nervous system lesion and repair were still unknown. Here, we performed an acute sciatic nerve injury model in adult rats and studied the dynamic changes of Spy1 expression in lumbar spinal cord. Temporally, Spy1 expression was increased shortly after sciatic nerve crush and peaked at day 2. Spatially, Spy1 was widely expressed in the lumbar spinal cord including neurons and glial cells. While after injury, Spy1 expression was increased predominantly in astrocytes and microglia, which were largely proliferated. Moreover, there was a concomitant up-regulation of CDK2 activity and down-regulation of p27. Collectively, we hypothesized peripheral nerve injury induced an up-regulation of Spy1 in lumbar spinal cord, which was associated with glial proliferation.

This study aimed to investigate the role of M3 acetylcholine receptor (M3-AChR) expression in airway remodeling. Additionally, we aimed to evaluate the effects of ipratropium bromide solution inhaled in an early phase of asthma on airway remodeling in ovalbumin (OVA)-sensitized and challenged mice. Thirty BALB/c mice were divided into three groups, namely, control group (saline sensitized/challenged mice), asthma group (OVA sensitized/challenged mice), and treatment group (OVA sensitized/challenged mice treated by ipratropium bromide). Pathological changes were detected by histological staining in the bronchopulmonary tissue of mice. WAt/Pbm (the airway wall area /basement membrane perimeter) ratio of the asthma group (25.37 ± 4.25) increased significantly (P < 0.05) when compared with that of the control (12.89 ± 1.71) and treatment group (15.82 ± 2.91). WAm/Pbm (smooth muscle wall area / basement membrane perimeter) ratio of the asthma group (7.58 ± 2.16) increased significantly (P < 0.05) when compared with that of the control (2.55 ± 0.72) and treatment group (3.36 ± 1.69). M3-AChR concentration increased in the treatment group (29.24 ± 3.59) and was significantly different (P < 0.05) from that of the control group (25.50 ± 1.83). During asthma treatment, SAMA can alleviate airway remodeling in murine model by lessening the thickness of bronchial walls and inhibiting the proliferation of smooth muscle cells. There were no obvious changes in M3-AChR density in the murine model of asthma characterized by airway remodeling. However, ipratropium bromide may up-regulate the expression of M3-AChR in bronchial walls of asthmatic murine model.

Background: The up-regulation of hepatic Golgi protein 73 (GP73) is associated with the progression of hepatocellular carcinoma (HCC). However, the exact mechanism and clinical values of its diagnosis and prognosis still need to be clarified. Objectives: To investigate the clinical values of abnormal liver or circulating GP73 expression and their effect on HCC diagnosis and prognosis. Materials and Methods: The expression of GP73 was investigated in 88 cancerous and self-control non-cancerous tissues using tissue microarrays with immunohisto- chemistry and was confirmed by Western blotting. Circulating GP73 levels were detected in the sera of 281 patients with liver diseases using enzyme-linked immunosorbent assay. Results: The levels of circulating GP73 expression in the HCC group were higher than those in any group of benign liver diseases or controls. No significant difference was found between GP73 expression and patients’ sex or age, tumor size, or AFP level except for those with hepatitis B virus (HBV) infection or distal metastasis (P < 0.05). The area under the receiver operating characteristic curve, sensitivity, and specificity for HCC diagnosis were 0.881, 78.34%, and 77.59% for GP73 levels over 70 μg/L or 0.754, 71.97%, and 84.48% for alpha-fetoprotein levels over 50 μg/L, respectively. The total incidence of GP73 plus alpha-fetoprotein was up to 87.26% for HCC. A positive GP73 result with brown particles was mainly located in the cytosol, with a few in the nucleus and none in the cell membrane, with abnormal expression in HCC tissues (480.7 ± 148.7) that was significantly higher (t = 10.730, P < 0.001) than those in their non-cancerous tissues (208.0 ± 66.1). The high GP73 expression in HCC was related to lymph node metastasis (χ 2 = 6.940, P = 0.008), gross classification ( χ 2 = 6.311, P = 0.012), HBV (χ 2 = 4.803, P = 0.028), tumor node metastasis staging (χ 2 = 4.887, P = 0.027), and five-year survival ( χ 2 = 5.206, P = 0.023). Conclusions: Abnormality of hepatic or circulating GP73 expression should be regarded as an emerging biomarker for HCC diagnosis and prognosis.

Hepatic annexin A2 (ANXA2) orchestrates multiple biologic processes and clinical symptoms and plays a key role in development, metastasis, and drug resistance of lethal hepatocellular carcinoma (HCC). However, the prognostic significance of ANXA2 for HCC has not been elucidated up to now. In this study, ANXA2 was frequently found to be up-regulated in HCC tissues compared with benign liver disease (BLD) tissues, which was consistent with the results in serum samples and tissue specimens of patients with HCC. Furthermore, ANXA2 expression was significantly correlated with differentiated degree, intrahepatic metastasis, portal vein thrombus, and tumor node metastasis (TNM) staging. More importantly, increased ANXA2 level was first confirmed to be closely associated with shortened overall survival of HCC (χ (2) = 12.872, P = 0.005) and identified as an independent prognostic factor (hazard ratio 1.338, 95 % confidence interval (CI) 1.013 ~ 1.766, P = 0.040), suggesting that ANXA2 up-regulation might represent an acquired metastasis phenotype of HCC, help to screen out high-risk population for HCC, or more effectively treat a subset of postsurgical HCC patients positive for ANXA2.

To investigate small interfering RNA (siRNA)-mediated inhibition of nuclear factor-kappa B (NF-κB) activation and multidrug-resistant (MDR) phenotype formation in human HepG2 cells.Total RNA was extracted from human HepG2 or LO2 cells. NF-κB/p65 mRNA was amplified by nested reverse transcription polymerase chain reaction and confirmed by sequencing. NF-κB/p65 was analyzed by immunohistochemistry. Specific-siRNA was transfected to HepG2 cells to knock down NF-κB/p65 expression. The effects on cell proliferation, survival, and apoptosis were assessed, and the level of NF-κB/p65 or P-glycoprotein (P-gp) was quantitatively analyzed by enzyme-linked immunosorbent assay.HepG2 cells express NF-κB/p65 and express relatively less phosphorylated p65 (P-p65) and little P-gp. After treatment of HepG2 cells with different doses of doxorubicin, the expression of NF-κB/p65, P-p65, and especially P-gp were dose-dependently upregulated. After HepG2 cells were transfected with NF-κB/p65 siRNA (100 nmol/L), the expression of NF-κB/p65, P-p65, and P-gp were downregulated significantly and dose-dependently. The viability of HepG2 cells was decreased to 23% in the combination NF-κB/p65 siRNA (100 nmol/L) and doxorubicin (0.5 μmol/L) group and 47% in the doxorubicin (0.5 μmol/L) group (t = 7.043, P0.001).Knockdown of NF-κB/p65 with siRNA is an effective strategy for inhibiting HepG2 cell growth by downregulating P-gp expression associated chemosensitization and apoptosis induction.

The hallmark of Sweet's syndrome (SS) is the infiltration of mature neutrophils in the upper dermis. We herein report a case of SS with multi-organ involvement. A 32-year-old man presented with fever, anemia and dyspnea. He was given antibiotics, without any improvements. Later, a number of erythematous lesions appeared, accompanied by deteriorating respiratory and cardiovascular functions. A diagnosis of SS was confirmed on a skin biopsy, and the patient was given corticosteroids, the dose of which was reduced after one month. The organ function subsequently deteriorated, and he ultimately died of multi-organ failure. Early recognition of SS with multi-organ involvement is important in patients with SS.

The temperature dependence of photoluminescence (PL) from a-C:H film deposited by CH3+ ion beam has been performed and an anomalous behavior has been reported. A transition temperature at which the PL intensity, peak position and full width at the half maximum change sharply was observed. It is proposed that different structure units. at least three, are responsible for such behavior. Above the transition point. increasing temperature will lead to the dominance of non-radiative recombination process, which quenches the PL overall and preferentially the red part, Possible emission mechanisms have been discussed. (C) 2002 Elsevier Science Ltd. All rights reserved.

The prognosis of hepatocellular carcinoma (HCC) is poor and its early diagnosis is of the utmost importance. This study aimed to investigate the values of glypican-3 (GPC-3) expression in the liver and sera and its gene transcription for diagnosis and monitoring of metastasis of HCC.Liver GPC-3 was analyzed in HCC tissues from 36 patients by immunohistochemistry and Western blotting. GPC-3 mRNA from circulating peripheral blood mononuclear cells from 123 HCC patients or 246 patients with other diseases or 36 HCC tissues was amplified by RT-PCR, quantitative real-time PCR, and confirmed by DNA sequencing. Circulating GPC-3 level was detected by ELISA.The increasing expression of GPC-3 was observed from non-cancerous to cancerous tissues, with brown granule-like staining localized in tumor parts of atypical hyperplasia and HCC formation. The positive rate of GPC-3 was 80.6% in HCC, 41.7% in their paracancerous tissues, and none in distal cancerous tissues (P0.001), with no significant difference in differentiation grade and tumor number except for size (Z=2.941, P=0.003). Serum GPC-3 was detected only in HCC (52.8%) and significant difference was found between GPC-3 and tumor size (X2=6.318, P=0.012) or HBV infection (X2=23.362, P0.001). Circulating GPC-3 mRNA was detected in 70.7% of HCC tissues, with relation to TNM stage, periportal cancerous embolus, and extra-hepatic metastasis (P0.001). The combination of circulating GPC-3, GPC-3 mRNA and alpha-fetoprotein is of complementary value for HCC diagnosis (94.3%).Both GPC-3 overexpression and GPC-3 mRNA abnormality could be used as markers for the diagnosis of HCC and monitoring its metastasis.

The micro-magnetic structures of Mn+ ion-implanted GaSb are studied using a magnetic force microscope (MFM). MFM images reveal that there are many magnetic domains with different magnetization directions in our samples. The magnetic domain structures and the magnetization direction of typical MFM patterns are analyzed by numeric simulation.

We evaluated the therapeutic efficacy of combined treatment of Aβ-immunization with simvastatin in an Alzheimer mouse model at age 22 months. DNA prime-adenovirus boost immunization induced modest anti-Aβ titers and simvastatin increased the seropositive rate. Aβ-KLH was additionally administered to boost the titers. Irrespective of simvastatin, the immunization did not decrease cerebral Aβ deposits but increased soluble Aβ and tended to exacerbate amyloid angiopathy in the hippocampus. The immunization increased cerebral invasion of leukocytes and simvastatin counteracted the increase. Thus, modest anti-Aβ titers can increase soluble Aβ and simvastatin may reduce inflammation associated with vaccination in aged Alzheimer mouse models.

Background Hepatocellular carcinoma (HCC) is characterized by a multi-cause, multi-stage and multi-focus process of tumor progression. Its prognosis is poor and early diagnosis is of utmost importance. This study was undertaken to investigate the dynamic expression of oncofetal antigen glypican-3 (GPC-3) and GPC-3 mRNA in hepatocarcinogenesis and to explore their early diagnostic value for HCC. Methods A hepatoma model was induced in male Sprague-Dawley rats with 0.05% 2-fuorenylacetamide and confirmed by hematoxylin and eosin staining and gamma-glutamyltransferase (GGT) expression. Total RNA was purified and transcribed into cDNA by reverse transcription. Fragments of the GPC-3 gene were amplified by nested RT-PCR, and confirmed by sequencing. GPC-3 was analyzed by immunohistochemistry, Western blotting or ELISA Results Positive GPC-3 expression showed as brown granule-like staining localized in the cytoplasm. Histological examination of hepatocytes revealed three morphological stages of granule-like degeneration, atypical hyperplasia (precancerous), and cancer formation, with a progressive increase of liver total RNA and GGT expression. The incidence of liver GPC-3 mRNA and GPC-3, and serum GPC-3 was 100%, 100% and 77.8% in the HCC group, 100%, 100%, and 66.7% in the precancerous group, 83.3%, 83.3%, and 38.9% in the degeneration group, and no expression in the liver or blood of the control group, respectively. There was a positive correlation between liver GPC-3 mRNA and total RNA level ( r =0.475, P r =1.0, P r = 0.994, P Conclusion Abnormal oncofetal antigen GPC-3 and GPC-3 mRNA expression in hepatocarcinogenesis may be promising molecular markers for early diagnosis of HCC.

Diabetic patients have a high risk of pulmonary disorders that are usually associated with restrictive impairment of lung function, suggesting a fibrotic process (van den Borst B, Gosker HR, Zeegers MP, Schols AM. Chest 138: 393–406, 2010; Ehrlich SF, Quesenberry CP Jr, Van Den Eeden SK, Shan J, Ferrara A. Diabetes Care 33: 55–60, 2010). The present study was undertaken to define whether and how diabetes causes lung fibrosis. Lung samples from streptozotocin-induced type 1 diabetic mice, spontaneously developed type 1 diabetic OVE26 mice, and their age-matched controls were investigated with histopathological and biochemical analysis. Signaling mechanism was investigated with cultured normal human lung fibroblasts in vitro. In both diabetes models, histological examination with Sirius red and hemotoxylin and eosin stains showed fibrosis along with massive inflammatory cell infiltration. The fibrotic and inflammatory processes were confirmed by real-time PCR and Western blotting assays for the increased fibronectin, CTGF, PAI-1, and TNFα mRNA and protein expressions. Diabetes also significantly increased NADPH oxidase (NOX) expression and protein nitration along with upregulation of angiotensin II (Ang II) and its receptor expression. In cell culture, exposure of lung fibroblasts to Ang II increased CTGF expression in a dose- and time-dependent manner, which could be abolished by inhibition of superoxide, NO, and peroxynitrite accumulation. Furthermore, chronic infusion of Ang II to normal mice at a subpressor dose induced diabetes-like lung fibrosis, and Ang II receptor AT1 blocker (losartan) abolished the lung fibrotic and inflammatory responses in diabetic mice. These results suggest that Ang II plays a critical role in diabetic lung fibrosis, which is most likely caused by NOX activation-mediated nitrosative damage.

Nano-ZnO was prepared by direct precipitation method with zinc chloride and sodium carbonate anhydrous as rawmaterials, and its particle size and dispersion were characterized by TEM. The effects of concentration and the ratio ofreactants and reaction temperature on its dispersion in aqueous solution were analyzed and the best reaction conditionswere as follows: reaction temperature 60 centi degree, ultrasonic vibration time 40 min, concentration of the reactant 0.5mol/l andmolar ratio of reactants 1:2 for the preparation. The cotton fabric and the polyester fabric which were both finished bypad-dry-cure process with antistatic finishing agent, which was compounded with nano-ZnO, were tested on theirantistatic property. According to the comparation between the cotton and the polyester treated fabrics on antistaticproperty, the results showed that the charge density of the polyester fabric was reduced to 9.5×10-8 C/m2 from 5.8×10-6C/m2, which was about 10 times as that of the cotton fabric.

A below 30K single-stage high-frequency multi-bypass pulse tube cryocooler(PTC) is introduced in this paper. At present, the lowest temperature of 27.46K has been achieved with input power of 100W and 23.8K with input power of 200W. Experiments show that if the area of multi-bypass and the length of inertance tube matching well, a better performance of PTC will be obtained.

Part of speech (POS) tagging is a basic subject for Chinese information processing. In general, the existence of multi-category words greatly affects the processing quality of corpora. High efficient methods and automatically correcting techniques for multi-category word tagging are the keys for improving tagging precision. In this paper, for part of speech correcting of multi-category word, a modeling method is introduced based on an incomplete decision table and two algorithms for attribute reduction and object reduction used for automatically acquiring correcting rules are presented based on attribute significance. The results of testing show the validity of our method for improving part of speech tagging precision in large corpora engineering.