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To overcome the deficiency of mean field method in introducing the intramolecular cyclization and the steric effects, the reactive bond fluctuation model was applied to study nonideal hyperbranched A2 + B3 polycondensation, which has high sensitivity of gelation to the concentration of monomers, the feed ratio and the reactivity of functional groups. Simulation demonstrated that the mean field theory overestimated hyperbranched polymerization especially at high reaction conversion in the system with low monomer concentration where the intramolecular cyclization and the steric hindrance play crucial influences on molecular weight, molecular weight distribution and gel point (GP). The dependences of GP on the monomer concentration, feed ratio, and the reactivity of groups are clearly shown. We further simulated a specific polycondensation system with aromatic terephthaloyl chloride (TCl, A2) and 1,1,1-tris(4-trimethylsiloxyphenyl)ethane (TMS-THPE, B3) (Macromolecules 2007, 40, 6846) using fitting technology, and estimated molecular weight, molecular weight distribution, GPs, and the conformation of hyperbanched polymer. It provides a feasible way to quantitatively understand hyperbranched polymerization with the reaction specificity. © 2010 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem, 2010

In this paper we establish two theta function identities with four parameters by the theory of theta functions. Using these identities we introduce common generalizations of Hirschhorn-Garvan-Borwein cubic theta functions, and also re-derive the quintuple product identity, one of Ramanujan’s identities, Winquist’s identity and many other interesting identities.

The Slit family of guidance cues binds to Roundabout (Robo) receptors to modulate neuronal, leukocytic, and endothelial migration. Slit-Robo signaling had been reported to function as chemoattractive signal for vascular endothelial cells during angiogenesis. In this study, we found that Robo1 was expressed in lymphatic endothelial cells to mediate the migration and tube formation of these cells upon Slit2 stimulation, which were specifically inhibited by the function-blocking antibody R5 to Slit2/Robo1 interaction. To further explore the lymphangiogenic effect and significance mediated by Slit-Robo signaling, we intercrossed Slit2 transgenic mice with a non-metastatic RIP1-Tag2 mouse tumor model, and found that transgenic overexpression of Slit2 significantly enhanced tumor lymphangiogenesis and subsequently promoted mesenteric lymph node metastasis of pancreatic islet tumors. Taken together, our findings reveal that through interacting with Robo1, Slit2 is a novel and potent lymphangiogenic factor and contributes to tumor lymphatic metastasis.

Purpose : To investigate the efficacy of capecitabine and ludartin in the treatment of colon cancer in mice. Methods: Mice model of colon cancer was used in this study. Quantitative real-time polymerase chain reaction (Qrt-PCR) was used to quantify the expression of vascular endothelial growth factor (VEGF) mRNA. Micro-vessel density was assessed using immunohistochemical analysis. Results : When administered separately, capecitabine and ludartin treatments significantly suppressed tumor growth in the mice model of colon cancer for 4 weeks, compared to control group. Coadministration of capecitabine and ludartin significantly inhibited tumor growth for 6 weeks (p < 0.05). Symptoms of colon cancer such as weight loss, skin discoloration and leukopenia were observed in untreated control group. However, these symptoms were completely absent in the group treated with combination of capecitabine and ludartin. The combined treatment also prevented colon cancer-induced increase in white blood cell (WBC) count, and increased median survival time of colon cancer mice from 38 to 55 days. Expression of VEGF in combination (capecitabine + ludartin) treatment group was significantly lower than in the control, i.e., untreated group (p ˂ 0.05). The combination treatment group also had significantly lower micro-vessel density in the tumor tissues, compared to the ntreated control mice (p < 0.05). Conclusion : These results show that a combination treatment of capecitabine and ludartin effectively inhibits colon tumor growth and angiogenesis in mice via a mechanism involving suppression of VEGF expression. Thus, capecitabine and ludartin combination is a potentially uitable treatment for colon cancer. Keywords : Colon cancer, Mice, Ludartin, Leukopenia, VEGF expression, Angiogenesis

The mechanisms for the three products ZrS+, ZrS 2 + and ZrOS+ of the title reaction have been studied by using B3LYP/6-311+G∗ and CCSD(T)/SDD+6-311+G∗ methods. It is found that both ZrS+ and ZrS 2 + formations involve the same O/S exchange process via a four-center transition state TS12 to form an intermediate IM2. Exception of that IM2 can dissociate into the ZrS+ product, a favorable intramolecular rearrangement mechanism associated with the ZrS 2 + formation has been identified, which explains why ZrS+ was excluded as a precusor for the ZrS 2 + formation and why the lower efficiency of the ZrS+ formation was observed in experiment. For the formation of ZrOS+, two parallel channels (path A and B) yielding their corresponding product isomer have been identified. Path B involving an insertion–elimination mechanism with a calculated barrier underestimated by ca. 25.0 kJ/mol should be attributed to the threshold of 114.8 ± 12.5 kJ/mol assigned in the experiment. But path A should make some contributions to the formation of ZrOS+ at elevated energy.

The Schröter formula is an important theta function identity. In this paper, we will point out that some well-known addition formulas for theta functions are special cases of the Schröter formula. We further show that the Hirschhorn septuple product identity can also be derived from this formula. In addition, this formula allows us to derive four remarkable theta functions identities, two of them are extensions of two well-known Ramanujan's identities related to the modular equations of degree 5. A trigonometric identity is also proved.

The reactions of NbS+ (3∑−, 1Γ) with COS have been studied using density functional theory at the B3LYP level: the O/S exchange reaction (NbS+ + COS → NbO+ + CS2), the S-transfer reaction (NbS+ + COS → NbS 2 + + CO) and the O-transfer reaction (NbS+ + COS → ONbS+ + CS). The different mechanisms on the triplet and singlet surfaces have been identified. It is found that the S-transfer reaction has two parallel reaction paths (path A and path B) with respective to two isomeric products ( NbS 2 + -1 and NbS 2 + -2), which may account, respectively, for the endothermic and the exothermic features of the product NbS 2 + cross-section observed in the experiment. The spin-forbidden reaction NbS+ (3∑−) + COS → NbS 2 + (1-A′) + CO was found to be energetically much more favorable than the spin-allowed reaction NbS+ (3∑−) + COS → NbS 2 + (3-A′) + CO. According to the identified reaction mechanisms, a triplet–singlet surface crossing is suggested. The larger activation barriers (23.7 and 59.5 kcal/mol) and the small probability of the formation of the preceding intermediate 3IM1 result in a much lower efficiency of the O/S exchange reaction and the O-transfer reaction of the 3∑− ground state of NbS+ with COS. For the O-transfer reaction, a triplet–singlet surface crossing may also exist.

BACKGROUND The mechanism of cerebral vasospasm following subarachnoid haemorrhage (SAH) is not understood. Here, we hypothesized that apoptosis of endothelial cells induced by p53 and its target gene em dash p53 upregulated modulator of apoptosis (PUMA) played an important role in development of cerebral vasospasm. We also observed the effects of a p53 inhibitor, pifithrin-alpha (PFT-alpha), on reducing the expression of p53 and PUMA, consequently decreasing the apoptosis of endothelial cells and alleviating cerebral vasospasm. METHODS Male Sprague-Dawley rats weighing 300-350 g were randomly divided into five groups: a control group (sham surgery), a SAH group, a SAH+dimethyl sulfoxide (DMSO) group, a SAH + PFT-alpha (0.2 mg/kg) group and a SAH + PFT-alpha (2.0 mg/kg) group. PFT-alpha was injected intraperitoneally immediately after SAH. Rats were sacrificed 24 hours after SAH. Western blot and immunohistochemical staining were used to detect the levels of p53, PUMA and caspase-3 protein. In addition, mortality and neurological scores were assessed for each group. Statistical significance was assured by analysis of variance performed in one way ANOVA followed by the Tukey test. The neurological and mortality scores were analyzed by Dunn's method and Fisher exact test, respectively. RESULTS After SAH, Western blot and immunohistochemical staining showed the levels of p53, PUMA and caspase-3 in the endothelial cells and the numbers of TdT mediated dUTP nick end labelling (TUNEL) positive endothelial cells were all significantly increased in the basilar arteries (P

Previous work has revealed that Helicoverpa armigera cathepsin B-like proteinase (HCB) is expressed in oocytes as well as fat bodies of pupae and adults. It plays key roles in the degradation of yolk proteins during embryogenesis and the decomposition of adult fat bodies of H. armigera. This study investigated the expression and function of HCB in larval hemocytes during larva–pupa metamorphosis. Results showed that the expression of HCB in hemocytes exhibited developmental stage specificity. No HCB was found in hemocytes from 5th-molting larvae. On the contrary, HCB was highly transcribed in the hemocytes from 6th–48-h larvae. Besides, it was abundantly translated in 6th–96-h larvae (prepupation). HCB is mainly expressed in plasmatocytes and granulocytes at both transcriptional and translational levels. The number of plasmatocytes and granulocytes markedly increased before pupation. In addition, hemocytes distributed in hematopoietic organs at early larval stage, then migrated to midgut and fat bodies that would undergo histolysis at later larval stage. These findings suggested that HCB is expressed in H. armigera larval hemocytes and involved in larva-pupa metamorphosis. Arch. Insect Biochem. Physiol. 64:164–174, 2007. © 2007 Wiley-Liss, Inc.

A slot antenna configuration is proposed for multi-standard multifunction mobile handset. The slot has a hybrid shape of the combination of a close-ended circle and two rectangles. The feeding structure of the slot is comprised of a 50 Ω microstrip connected to a circular patch and an open-ended strip, a T-shaped step is adopted to connect the circular patch and the microstrip. The proposed antenna were fabricated by two methods, one of which is corroding double-layered copper covered FR4 board by acid, and the other is cutting copper foil. The method of cutting copper foil has the virtues of low cost and easy fabrication, it works well below 6GHz. The measured −6dB bandwidth of the proposed antenna covers 0.69–0.975 GHz and 2.09–3.32GHz.

Liver kinase B1 (LKB1) has been identified as a critical modulator involved in cell proliferation and polarity. The purpose of the current study was to characterize the expression pattern of LKB1 and assess the clinical significance of LKB1 expression in pancreatic ductal adenocarcinoma (PDAC) patients. LKB1 mRNA expression which was analyzed in 32 PDAC lesions and matched non-tumor tissues, was downregulated in 50% (16/32) of PDAC lesions. Similar results were also obtained by analyzing three independent datasets from Oncomine. Protein expression of LKB1 was significantly reduced in 6 PDAC cell lines and downregulated in 31.3% (10/32) of PDAC lesions compared to matched non-tumorous tissues, as determined by Western blot analysis. Additionally, tissue microarray containing 205 PDAC specimens was evaluated for LKB1 expression by IHC and demonstrated that reduced expression of LKB1 in 17.6% (36/205) of PDAC tissues was significantly correlated with clinical stage, T classification, N classification, liver metastasis and vascular invasion. Importantly, Kaplan-Meier survival and Cox regression analyses were executed to evaluate the prognosis of PDAC and found that LKB1 protein expression was one of the independent prognostic factors for overall survival of PDAC patients.

// Shu-Heng Jiang 1, 2, * , Yang Wang 1, 2, 4, * , Jian-Yu Yang 3, * , Jun Li 2, * , Ming-Xuan Feng 5 , Ya-Hui Wang 1, 2 , Xiao-Mei Yang 2 , Ping He 2 , Guang-Ang Tian 2 , Xiao-Xin Zhang 2 , Qing Li 1, 2 , Xiao-Yan Cao 2 , Yan-Miao Huo 3 , Min-Wei Yang 3 , Xue-Liang Fu 3 , Jiao Li 3 , De-Jun Liu 3 , Miao Dai 7 , Shan-Yun Wen 7 , Jian-Ren Gu 1, 2 , Jie Hong 6 , Rong Hua 3 , Zhi-Gang Zhang 2 , Yong-Wei Sun 3 1 Shanghai Medical College of Fudan University, Shanghai, P.R. China 2 State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China 3 Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China 4 Department of Urology, Shanghai No.5 People’s Hospital, Fudan University, Shanghai, P.R. China 5 Department of Liver Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China 6 Division of Gastroenterology and Hepatology, Ren Ji Hospital, Shanghai Institution of Digestive Disease, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory of Oncogene and Related Genes, Shanghai Jiao-Tong University School of Medicine, Shanghai, P.R. China 7 Department of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, P.R. China * These authors contributed equally to this work Correspondence to: Yong-Wei Sun, e-mail: syw0616@126.com Zhi-Gang Zhang, e-mail: zzhang@shsci.org Rong Hua, e-mail: lordhuarong@sohu.com Jie Hong, e-mail: jiehong97@gmail.com Keywords: EDIL3, prognosis, tumor growth, anoikis, pancreatic cancer Received: June 16, 2015 Accepted: November 28, 2015 Published: December 28, 2015 ABSTRACT Epidermal Growth Factor-like repeats and Discoidin I-Like Domains 3 (EDIL3), an extracellular matrix (ECM) protein associated with vascular morphogenesis and remodeling, is commonly upregulated in multiple types of human cancers and correlates with tumor progression. However, its expression pattern and underlying cellular functions in pancreatic ductal adenocarcinoma (PDAC) remain largely unexplored. In current study, we observed that expression of EDIL3 was significantly up-regulated in PDAC compared with normal controls in both cell lines and clinical specimens. In addition, elevated EDIL3 expression was positively correlated with patients’ TNM stage and T classification. Kaplan-Meier analysis indicated that high EDIL3 expression was significantly associated with shorter overall survival times in PDAC patients. Multivariate Cox regression analysis confirmed EDIL3 expression, age, lymph node metastasis and histological differentiation as independent prognostic factors in PDAC. Knockdown of EDIL3 showed no significant influence on cell viability, migration, invasion and starvation-induced apoptosis, but compromised anoikis resistance and anchorage independent tumor growth of PDAC cells. Meanwhile, treatment with recombinant EDIL3 protein markedly promoted anoikis resistance and anchorage independent tumor growth. Mechanistically, we demonstrated that altered protein expression of Bcl-2 family might contribute to the oncogenic activities of EDIL3. In conclusion, this study provides evidences that EDIL3 is a potential predictor and plays an important role in anchorage independent tumor growth of PDAC and EDIL3-related pathways might represent a novel therapeutic strategy for treatment of pancreatic cancer.

Liver kinase B1 (LKB1) has been identified as a critical modulator involved in cell proliferation and polarity. The purpose of the current study was to characterize the expression pattern of LKB1 and assess the clinical significance of LKB1 expression in pancreatic ductal adenocarcinoma (PDAC) patients. LKB1 mRNA expression which was analyzed in 32 PDAC lesions and matched non-tumor tissues, was downregulated in 50% (16/32) of PDAC lesions. Similar results were also obtained by analyzing three independent datasets from Oncomine. Protein expression of LKB1 was significantly reduced in 6 PDAC cell lines and downregulated in 31.3% (10/32) of PDAC lesions compared to matched non-tumorous tissues, as determined by Western blot analysis. Additionally, tissue microarray containing 205 PDAC specimens was evaluated for LKB1 expression by IHC and demonstrated that reduced expression of LKB1 in 17.6% (36/205) of PDAC tissues was significantly correlated with clinical stage, T classification, N classification, liver metastasis and vascular invasion. Importantly, Kaplan-Meier survival and Cox regression analyses were executed to evaluate the prognosis of PDAC and found that LKB1 protein expression was one of the independent prognostic factors for overall survival of PDAC patients.

The interactions of bovine serum albumin (BSA) with five novel silicon (N) phthalocyanines(SiPcl-5) axially modified by nucleosides (cytidine, 5-N-cytidine, methyl cytidine, uridine and methyl uridine) derivatives were studied by fluorescence spectroscopy. The results show that there are strong interactions between these silicon phthalocyanines and BSA with a binding constant of (4.90-83.18) x 10(5) mol(-1) x L. Therefore, the non-covalent BSA conjugate of bis(2', 3'-O-isopropyl-cytidine-oxy) phthalocyaninatosilicon(IV) (SiPc1) was further been prepared. The molar ratio of phthalocyanine to albumin was found to be 1:1 for the obtained SiPcl-BSA conjugate. The absorption spectra of SiPc1 and SiPc1-BSA in the visible region have no significant difference, both showing an Q-band maximum at about 686 nm. It indicates that the spectroscopic characteristics of SiPc1 are not affected by binding to albumin. The SiPcl-BSA conjugate exhibits high photodynamic activity against human hepatoma cell line HepG2 with an IC50 value of 3.0 x 10(-7) mol x L(-1). By comparsion, SiPc1-BSA has a higher photodynamic activity than SiPc1 (in PBS formation, IC50 = 7.0 x 10(-7) mol x L(-1)), which can be attributed to its higher cellular uptake.

Two new heteropoly tungstovanadate derivatives, [Fe(phen)3]2[W10.5V4.5O42]·3H2O (1) and [Fe(phen)3]2[W10V5O42].6H2O (2) (phen=1,10′-phenanthroline), have been synthesized under hydrothermal conditions by using different starting materials, and characterized by elemental analysis, IR, ESR, XPS, TGA and single-crystal X-ray diffraction analysis. Crystal data for compound 1: C72H54Fe2N12O45V4.5W10.5, monoclinic, space group C2/c, a = 30.244 ( 9 ) A , b = 13.586 ( 3 ) A , c = 24.707 A , β = 99.882 (8)°, V = 10002 (5) A3, Z = 4 ; for compound 2, C72H60Fe2N12O48V5W10, monoclinic, space group C2/c, a = 30.246 (6) A, b = 13.909 ( 3 ) A , c = 25.329 (5) A, β = 100.34 (3)°, V = 10483 (4) A3, Z = 4 . The crystal structure analysis reveals that both polyoxoanions are decorated with the [Fe(phen)3]2+ cations, and that they have analogous structure to each other with slightly different packing modes of the polyoxoanions, [Fe(phen)3]2+ cations and water molecules. They are further linked to form two-dimensional (2D) supramolecular networks through extensive hydrogen bonding.

Cathepsin B-like proteinase (HCB, EC 3.4.22.1) is expressed in Helicoverpa armigera oocytes and adult fat bodies. Previous work has revealed that HCB plays a key role in the degradation of yolk proteins during embryogenesis. This study investigated the function and regulatory activation of HCB in adult fat bodies during aging and oogenesis. The HCB transcript was detected at all stages from larval to adult fat bodies with Northern blot analysis. Pro-HCB was also detected in fat bodies at these stages with an immunoblot assay using a monoclonal antibody against HCB. However, mature HCB and its activity were only detected in fat bodies of pre-adults and adults. This evidence suggested that HCB is regulated post-translationally by activation of the pro-enzyme during the pupa-adult metamorphosis. The activation of HCB was coupled with the expression of hormone receptor 3 (HHR3), and was up-regulated by the ecdysteroid agonist, RH-2485, suggesting that HCB activation is related to the ecdysone regulatory system. The decomposition of the adult fat bodies during aging and oogenesis was found to occur via programmed cell death, in which HCB took part.

A new member of antimicrobial peptide genes of the penaeidin family, Ch-penaeidin, has been cloned from the haemocytes of Chinese shrimp, Fenneropenaeus chinensis, by reverse transcription PCR (RT-PCR), 3'-rapid amplification of cDNA end (3'-RACE) and smart cDNA methods. The Ch-penaeidin cDNA was 655 bp and the open reading frame of the cDNA encoded a 71 amino acid peptide. Ch-penaeidin contained a putative NH2-terminal signal Sequence (1-19) followed by a mature peptide (20-71). The sequence identify with other penaeidins from Litopenaeus vannamei and Litopenaeus setiferus is between 48% and 71%. The signal sequence of Ch-penaeidin is almost completely identical to that of other penaeidins, while differing relatively in the N-terminal domain of the mature peptide. Ch-penaeidin was designated as a novel member of class penaeidin 3 according to phylogenetic analysis. The Mature peptide. with a predicted molecular weight of 5589.32 Da, and a pI of 9.77, has eight positively charged amino acids and no negatively charged amino acids. The expression and distribution of Ch-penaeidin in Unchallenged shrimps were studied by RT-PCR, Northern blot and in situ hybridisation. The results showed that the Ch-penaeidin transcripts were detected in haemocytes (granular haemocytes), heart, gill, intestine, and subcuticular epithelia of the shrimp. and that Ch-penaeidin was constitutively expressed mainly in haemocytes. (C) 2003 Elsevier Ltd. All rights reserved.

Background & Aims Desmoplasia and poor vascularity cause severe metabolic stress in pancreatic ductal adenocarcinomas (PDACs). Serotonin (5-HT) is a neuromodulator with neurotransmitter and neuroendocrine functions that contributes to tumorigenesis. We investigated the role of 5-HT signaling in the growth of pancreatic tumors. Methods We measured the levels of proteins that regulate 5-HT synthesis, packaging, and degradation in pancreata from Kras G12D/+ /Trp53 R172H/+ /Pdx1-Cre (KPC) mice, which develop pancreatic tumors, as well as in PDAC cell lines and a tissue microarray containing 81 human PDAC samples. We also analyzed expression levels of proteins involved in 5-HT synthesis and degradation by immunohistochemical analysis of a tissue microarray containing 311 PDAC specimens, and associated expression levels with patient survival times. 5-HT level in 14 matched PDAC tumor and non-tumor tissues were analyzed by ELISA. PDAC cell lines were incubated with 5-HT and cell survival and apoptosis were measured. We analyzed expression of the 5-HT receptor HTR2B in PDAC cells and effects of receptor agonists and antagonists, as well as HTR2B knockdown with small hairpin RNAs. We determined the effects of 5-HT stimulation on gene expression profiles of BxPC-3 cells. Regulation of glycolysis by 5-HT signaling via HTR2B was assessed by immunofluorescence and immunoprecipitation analyses, as well as by determination of the extracellular acid ratio, glucose consumption, and lactate production. Primary PDACs, with or without exposure to SB204741 (a selective antagonist of HTR2B), were grown as xenograft tumors in mice, and SB204741 was administered to tumor-bearing KPC mice; tumor growth and metabolism were measured by imaging analyses. Results In immunohistochemical analysis of a tissue microarray of PDAC specimens, increased levels of TPH1 and decreased level of MAOA, which regulate 5-HT synthesis and degradation, correlated with stage and size of PDACs and shorter patient survival time. We found levels of 5-HT to be increased in human PDAC tissues compared with non-tumor pancreatic tissues, and PDAC cell lines compared with non-transformed pancreatic cells. Incubation of PDAC cell lines with 5-HT increased proliferation and prevented apoptosis. Agonists of HTR2B, but not other 5-HT receptors, promoted proliferation and prevented apoptosis of PDAC cells. Knockdown of HTR2B in PDAC cells, or incubation of cells with HTR2B inhibitors, reduced their growth as xenograft tumors in mice. We observed a correlation between 5-HT and glycolytic flux in PDAC cells; levels of metabolic enzymes involved in glycolysis, the phosphate pentose pathway, and hexosamine biosynthesis pathway increased significantly in PDAC cells following 5-HT stimulation. 5-HT stimulation led to formation of the HTR2B–LYN–p85 complex, which increased PI3K–Akt–mTOR signaling and the Warburg effect by increasing protein levels of MYC and HIF1A. Administration of SB204741 to KPC mice slowed growth and metabolism of established pancreatic tumors and prolonged survival of the mice. Conclusions Human PDACs have increased levels of 5-HT, and PDAC cells increase expression of its receptor, HTR2B. These increases allow for tumor glycolysis under metabolic stress and promote growth of pancreatic tumors and PDAC xenograft tumors in mice.

Ovarian cancer remains the disease with the highest associated mortality rate of gynecologic malignancy due to cancer metastasis. Rearrangement of actin cytoskeleton by cytoskeleton protein plays a critical role in tumor cell metastasis. MICAL-L2, a member of MICAL family, can interact with actin-binding proteins, regulate actin cross-linking and coordinate the assembly of adherens junctions and tight junctions. However, the roles of MICAL-L2 in tumors and diseases have not been explored. In this study, we found that MICAL-L2 protein is significantly up-regulated in ovarian cancer tissues along with FIGO stage and associated with histologic subgroups of ovarian cancer. Silencing of MICAL-L2 suppressed ovarian cancer cell proliferation, migration and invasion ability. Moreover, silencing of MICAL-L2 prevented nuclear translocation of β-catenin, inhibited canonical wnt/β-catenin signaling and induced the mesenchymal-epithelial transition (MET). Taken together, our data indicated that MICAL-L2 may be an important regulator of epithelial-mesenchymal transition (EMT) in ovarian cancer cells and a new therapeutic target for interventions against ovarian cancer invasion and metastasis.

Dermatopontin (DPT), a tyrosine-rich, acidic matricellular protein, has been implicated in several human cancers. However, its biological functions and molecular mechanisms in cancer progression, particular hepatocellular carcinoma (HCC), remain unknown. We demonstrated that DPT was significantly down-regulated in 202 HCC clinical samples and that its expression level was closely correlated with cancer metastasis and patient prognosis. The overexpression of DPT dramatically suppressed HCC cell migration in vitro and intrahepatic metastasis in vivo. We further revealed that the down-regulation of DPT in HCC was due to epigenetic silencing by promoter DNA methylation. And the inhibitory effects of DPT on HCC cell motility were associated with dysregulated focal adhesion assembly, decreased RhoA activity and reduced focal adhesion kinase (FAK) and c-Src tyrosine kinase (Src) phosphorylation, and all of these alterations required the involvement of integrin signaling. Furthermore, we determined that the inhibitory effects of DPT on HCC cell motility were primarily mediated through α3β1 integrin. Our study provides new evidence for epigenetic control of tumor microenvironment, and suggests matricellular protein DPT may serve as a novel prognostic marker and act as a HCC metastasis suppressor.

CCN6/Wnt1-inducible signaling protein-3 (CCN6/WISP3) is a cysteine-rich protein that belongs to the CCN (Cyr61, CTGF, Nov) family of matricellular proteins, which are often dysregulated in cancers. However, the functional role and clinical significance of WISP3 in gastric cancer remain unclear. In this study, we found that silencing of WISP3 suppressed gastric cancer cell proliferation, migration and invasion. Cell adhesion to collagens (collagen I and IV), but not to fibronectin, were significantly inhibited by silencing of WISP3. Furthermore, silencing of WISP3 prevented β-catenin transferring from cell cytoplasm to nuclear, and suppressed canonical Wnt/β-catenin signaling and its downstream target genes, cyclin D1 and TCF-4. By immunohistochemical analysis of 379 patients, we found that the expression of WISP3 is closely associated with gastric cancer size and tumor invasion, and indicates a poor prognosis in both test cohort (253 patients) and validation cohort (126 patients). Moreover, the expression of WISP3 was positively correlated with the expression of cyclin D1 and TCF-4 in gastric cancer tissues. Taken together, our data suggests that WISP3 might be a promising prognostic factor and WISP3-Wnt/β-catenin axis may be a new therapeutic target for the intervention of gastric cancer growth and metastasis.

Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality, and is characterized by high potential for metastasis and recurrence. The outcome of it is still poor due to lacking of targeted therapeutic strategies. There is an urgent need to find new therapeutic targets for interventions against HCC metastasis and recurrence. In the present study, we found cytohesin-3, a member of the cytohesin family, was upregulated in HCC tissues, and its expression was negatively correlated with the overall survival and relapse-free survival of HCC patients. Further clinicopathological correlation analysis revealed that cytohesin-3 expression was related with tumor size and vascular invasion. And in vitro studies revealed that knock-down of cytohesin-3 suppressed HCC cells proliferation and migration. These results suggest that cytohesin-3 may act as a novel prognostic factor of HCC, and it might also be useful to exploit targeted therapeutic drugs against HCC growth and metastasis.

Endometrial carcinoma (EC) is the most common gynecologic cancer worldwide and is one of the leading causes of death in women. Therefore, it is urgent to elucidate the pathological mechanisms of EC. SERPINA3 is a member of the serpin super-family of protease inhibitors. Its aberrant expression has been observed in various tumor cells. However, its clinical significance and biological function in endometrial cancer remains unknown. In the present study, we demonstrated that SERPINA3 expression was significantly up-regulated in EC samples and was closely correlated with lower differentiation, higher stage, positive lymph node or vascular thrombosis and negative estrogen receptor (ER), indicating a poor prognosis. We then demonstrated that SERPINA3 promoted EC cells proliferation by regulating G2/M checkpoint in cell cycle and inhibited cells apoptosis, and we further uncovered that the pro-proliferative effect of SERPINA3 on EC was likely ascribed to the activation of MAPK/ERK1/2 and PI3K/AKT signaling. The results of our study may provide insight into the application of SERPINA3 as a novel predictor of clinical outcomes and a potential therapeutic target of EC.

Endometrial cancer (EC) is one of the most common female malignancies. The patients with high-risk factors may have poor prognosis. Therefore, there is an urgent need to find a new molecule to more accurately predict survival of patients. Leucine-rich-alpha-2-glycoprotein1 (LRG1), one of leucine-rich repeat family, was closely associated with cancer metastasis and poor prognosis. The biological functions and the expression level of LRG1 remain obscure in EC. In this study, by immunohistochemical analysis of 242 EC patient tissues, we found that LRG1 expression was associated with stage and lymphatic metastasis in both test cohort (133 patients) and validation cohort (109 patients). Furthermore, to investigate the prognostic value of LRG1 in endometrial carcinoma, we analyzed the correlation between variables and overall survival with Cox proportional hazard regression. The result showed that LRG1 was an independent prognostic factor for overall survival of endometrial carcinoma patients. To further evaluate the prognostic efficiency of LRG1 in endometrial carcinoma, we compared the sensitivity and specificity of LRG1 in endometrial carcinoma prognosis by logistic regression. The result showed that LRG1 combining with other clinicopathological risk factors was a stronger prognostic model than clinicopathological risk factors alone or their combination. Thus, LRG1 potentially offered clinical value in directing personal treatment for endometrial carcinoma patients.

Mammalian enabled (MENA), usually known as a direct regulator of microfilament polymerization and bundling, promotes metastasis in various cancers. Here we focus on the role of MENA in hepatocellular carcinoma (HCC) metastasis and the relevant mechanism from the view of RhoA activity regulation. By HCC tissue microarray analysis, we found that MENA expression was positively associated with satellite lesions (P

Embryonic stem (ES) cells are widely used for different purposes, including gene targeting, cell therapy, tissue repair, organ regeneration, and so on. However, studies and applications of ES cells are hindered by ethical issues regarding cell sources. To circumvent ethical disputes, great efforts have been taken to generate ES cell-like cells, which are not derived from the inner cell mass of blastocyst-stage embryos. In 2006, Yamanaka et al. first reprogrammed mouse embryonic fibroblasts into ES cell-like cells called induced pluripotent stem (iPS) cells. About one year later, Yamanaka et al. and Thomson et al. independently reprogrammed human somatic cells into iPS cells. Since the first generation of iPS cells, they have now been derived from quite a few different kinds of cell types. In particular, the use of peripheral blood facilitates research on iPS cells because of safety, easy availability, and plenty of cell sources. Now iPS cells have been used for cell therapy, disease modeling, and drug discovery. In this review, we describe the generations, applications, potential issues, and future perspectives of iPS cells.

Although significant advances have recently been made in the diagnosis and treatment of cervical carcinoma, the long-term survival rate for advanced cervical cancer remains low. Therefore, an urgent need exists to both uncover the molecular mechanisms and identify potential therapeutic targets for the treatment of cervical cancer. MicroRNAs (miRNAs) have important roles in cancer progression and could be used as either potential therapeutic agents or targets. miR-506 is a component of an X chromosome-linked miRNA cluster. The biological functions of miR-506 have not been well established. In this study, we found that miR-506 expression was downregulated in approximately 80% of the cervical cancer samples examined and inversely correlated with the expression of Ki-67, a marker of cell proliferation. Gain-of-function and loss-of-function studies in human cervical cancer, Caski and SiHa cells, demonstrated that miR-506 acts as a tumor suppressor by inhibiting cervical cancer growth in vitro and in vivo. Further studies showed that miR-506 induced cell cycle arrest at the G1/S transition, and enhanced apoptosis and chemosensitivity of cervical cancer cell. We subsequently identified Gli3, a hedgehog pathway transcription factor, as a direct target of miR-506 in cervical cancer. Furthermore, Gli3 silencing recapitulated the effects of miR-506, and reintroduction of Gli3 abrogated miR-506-induced cell growth arrest and apoptosis. Taken together, we conclude that miR-506 exerts its anti-proliferative function by directly targeting Gli3. This newly identified miR-506/Gli3 axis provides further insight into the pathogenesis of cervical cancer and indicates a potential novel therapeutic agent for the treatment of cervical cancer.

Lumican is a dermatan sulfate proteoglycan highly expressed in connective tissue and has the ability to regulate collagen fibril assembly. Previous studies have shown that lumican is involved in wound healing, but the precise effects of lumican on reepithelialization and wound contraction, the two pivotal aspects of skin wound healing, have not been investigated. Here we explored the roles of lumican in fibroblast contractility, a main aspect of skin wound healing, by adopting mice skin wound healing model and the corresponding in vitro cellular experiments. Our results showed that lumican can promote skin wound healing by facilitating wound fibroblast activation and contraction but not by promoting keratinocyte proliferation and migration. Silencing of integrin α2 completely abolished the pro-contractility of lumican, indicating lumican enhances fibroblast contractility via integrin α2. Our study for the first time demonstrated that lumican can affect fibroblast’s mechanical property, which is pivotal for many important pathological processes, such as wound healing, fibrosis, and tumor development, suggesting that lumican might have a potential to be used to modulate these processes.

Embryonic stem (ES) cells are used in various fields for diverse purposes, including gene targeting, cell therapy, tissue repair, organ regeneration, and so on. However, studies on and applications of ES cells are hindered by ethical disputes regarding cell source. To circumvent ethical issues, scientists have attempted to generate ES celllike cells, which are not derived from the inner cell mass of blastocyst-stage embryos. In 2006, Yamanaka first reprogrammed mouse embryonic fibroblasts into ES cell-like cells, which were called induced pluripotent stem (iPS) cells. Nearly a year later, the Yamanaka and Thomson laboratories independently reprogrammed human somatic cells into iPS cells. Since the establishment of the first iPS cell line, iPS cells have been derived from a number of different cell types and have been used for cell therapy, human disease modeling, and drug discovery. The use of peripheral blood facilitates research on iPS cells and enables the establishment of patient-specific iPS cells. With the improvement in iPS cell technology, clinical therapy based on iPS cells will rapidly develop.

The ill-posed problem of attempting to recover the temperature functions from one measured transient data temperature at some interior point of a one-dimensional semi-infinite conductor when the governing linear diffusion equation is of fractional type is discussed. A simple regularization method based on Dirichlet kernel mollification techniques is introduced. We also proposea priorianda posterioriparameter choice rules and get the corresponding error estimate between the exact solution and its regularized approximation. Moreover, a numerical example is provided to verify our theoretical results.

An inverse source identification problem for a time fractional diffusion equation is discussed. The unknown heat source is supposed to be space dependent only. Based on the use of Green’s function, an effective numerical algorithm is developed to recover both the intensities and locations of unknown point sources from final measurements. Numerical results indicate that the proposed method is efficient and accurate.

The investigation of the magnetic field produced by power lines has drawn a lot of attention from researchers. Since sharing space by buried power lines and pipelines has become commonplace, it is of interest to investigate the influence of the pipeline. In this paper, we study the change of the magnetic field produced by buried cables, due to an additional steel pipe nearby. A Fourier series technique is used to calculate the magnetic field. An iterative procedure is employed to handle the nonlinear characteristics of the steel pipe and to determine the varying permeability in it. The calculated results of the magnetic field are compared with those produced by buried cables without the additional pipe. The comparison shows that the steel pipe close to buried cables may significantly alter the magnetic field.

Autophagy is an evolutionarily conserved cellular process that primarily participates in lysosome-mediated protein degradation. Although autophagy is a cytoplasmic event, how epigenetic pathways are involved in the regulation of autophagy remains incompletely understood. Here, we found that H2B monoubiquitination (H2Bub1) is down-regulated in cells under starvation conditions and that the decrease in H2Bub1 results in the activation of autophagy. We also identified that the deubiquitinase USP44 is responsible for the starvation-induced decrease in H2Bub1. Furthermore, the changes in H2Bub1 affect the transcription of genes involved in the regulation of autophagy. Therefore, this study reveals a novel epigenetic pathway for the regulation of autophagy through H2Bub1.

This paper presents a simple computational method for predicting the magnetic field above ground, generated by an underground three-phase pipe-type cable. In the computation, an approximation is made to simplify the problem, a Fourier series technique and an iterative procedure are employed to handle the nonlinear B-H characteristic of the steel pipe. To validate the computational method, measurements were made and the numerical results are compared with the measurement data. Also, data of magnetic fields generated by the pipe type cable are compared with those due to the cable in the absence of the pipe. The advantages and disadvantages of this simple method are discussed. >

In this paper, the problem of reconstruction of the solution of nonlinear ill-posed problem F(x)= y by Tikhonov regularization method is considered, where instead of y noisy data yδ with ∥y − yδ∥≤ δ are given and F:D(F)⊂X→Y is a nonlinear operator. A priori parameter choice rule and two a posteriori parameter choice rules are suggested. The order optimal convergence rate is O((−logδ)−p) under logarithmic-type source conditions. Moreover, we apply this method to an inverse boundary identification problem for verifying some of the theoretical results.

To investigate and analyze the situation of urban and rural neglected children aged 3 - 6, in China, so as to provide basis for the analysis and comparison on relevant risk factors.1163 urban children aged 3 - 6 (with 49.6% males and 4.5% with minority ethnicity) were investigated from 25 cities of 14 provinces, autonomous regions and municipalities in the whole country. Multi-stage stratified cluster sampling method was used. Again, using the same sampling method, 4096 rural children (of whom 50.6% were males with 6.2% as minorities) were chosen from 26 cities of 10 provinces or municipalities. Identification of children being neglected was based on "Child Neglect Evaluation Norms of Children Aged 3 - 6 Years in Urban/Rural China". SPSS-Windows 13.0 was employed for data analysis. Scores, frequency/degrees, age, sex and types (physical, emotional, educational, safety, medical and social) of children under negligence on every group of the regions, were calculated. χ(2) test (Chi-Square) and Analysis of variance (ANOVA) were processed to determine the significance of their differences.The overall frequencies of negligence were 28.0% and 53.7% respectively among the urban and rural children aged 3 - 6, while the total degrees of negligence were 42.2 and 44.4 respectively. Significant difference was found between children from the urban and the rural areas (P0.05). Significant difference was also found between urban and rural children on every age group (P0.05). The frequencies of negligence among males were 32.6% and 55.9% respectively in urban and rural areas while among females, the figures appeared to be 23.7% and 51.6% respectively. The degrees of negligence were 42.7 and 44.6 among male while 41.8 and 44.3 among female children, in the urban or rural areas. Significant differences were found on male or female between urban and rural groups (P0.05). Frequencies of negligence in urban children aged 3 - 6 for the six types were from 5.1% to 12.9%, with the frequency in rural areas as 13.1% - 26.6%. Significant difference was found between urban and rural group for any other type (P0.05), in addition to the safety type. The degrees of negligence in urban children aged 3 - 6 for the different type were between 39.4 and 43.4, while in the rural areas as from 36.5 to 48.2, with significant difference for every type (P0.05). The degrees of negligence related to education, emotion, or physical strength were more serious on children from the urban than from the rural areas. The highest frequency of child negligence was seen in the single-parent families on both urban and rural groups (42.9% and 60.0% respectively), with no significant difference found (P0.05). The urban and rural children aged 3 - 6 were mainly involved in single item of negligence, with incidence rates as 16.5% and 22.7% and proportions as 58.9% and 45.1% respectively, despite the factors as age or sex.There were large differences on the situation of negligence between the urban and rural children aged 3 - 6. The frequencies and degrees of negligence in every age group and different sex for children living in the rural areas were higher than those urban children. The frequency of negligence among boys was higher than girls for both urban and rural areas. The rural children had suffered more serious negligence than the urban children at any other type, in addition to the 'safety'. Both urban and rural children had the highest frequency of negligence in single-parent family, and were mainly suffered from single item of negligence.

To explore the status of child neglect among rural areas children aged 0 - 6 years in China.A total of 7411 rural children aged 0 - 6 years old who were composed of two age groups (3315 children aged 0 - 2 years old and 4096 children aged 3 - 6 years old) were multistage stratified randomly sampled from 84 villages which were representative of 10 provinces of China, in accordance with sex and age in November 2010. To identify the child neglect based on the Neglect Norms for Children Aged 0 to 2 and 3 to 6 Years Old in Rural Areas of China, SPSS 13.0 was employed for analyzing neglect frequency and degree for every group of different age, sex and neglect type (including physical, emotional, educational, medical, safety and social neglects). χ(2) test and analysis of variance were also used.The degree of child neglect for the children aged 0 - 2 years old was 45.01 ± 7.56, the neglect frequency was 54.9% (1819/3315); the degree of child neglect for the children aged 3 - 6 years old was 44.42 ± 7.57, the neglect frequency was 53.8% (2203/4096). The neglect frequency of children aged 0, 1, 2 years old were 58.5% (654/1117), 52.2% (597/1144), 53.9% (568/1054) (P0.05). For children aged 3 - 6 years old, the degrees of emotional and safety neglect for males (44.60 ± 7.86, 36.82 ± 9.03) were higher than females (44.03 ± 7.72, 36.25 ± 9.05) (P0.05); and the frequencies of emotional and social neglect for males (16.8% (349/2072), 28.3% (586/2072)) were also higher than females (14.1% (286/2024), 24.8% (503/2024)) (P0.05). All children of two age groups suffered neglect mainly on one of the six neglect types (incidences were 20.6% (683/3315) and 22.7% (931/4096)). For 0-2 age groups, the higher neglect frequencies happened in the single-parent family and the remarried family (62.5% (15/24) and 63.2% (12/19)), but for children aged 3 - 6 years old groups, it happened in the single-parent family (60.0%, 27/45).Degree and frequency of child neglect among children aged 0 to 6 years old in the rural areas of China are high, and we should find out risk factors and provide efficient prevention measures.

To explore the status of child neglect among urban areas children and adolescents aged 3 - 17 years in China.Using multi-stage stratified cluster sampling method, 8001 children and adolescents were recruited from 30 cities of 14 provinces in December 2008. The investigation was carried based on The 3 - 6 years old children Neglect Norms of city in China and The 6 - 17 years old children Neglect Norms of city in China. SPSS 13.0 was employed for analyzing neglect rate and degree for group of areas, age, sex and neglect type (including neglect of physical, emotional, educational, medical, safety and social).The degrees of child neglect for urban children aged 3 - 6 (children aged 6 were not in school), 6 - 8 (children aged 6 were school children), 9 - 11, 12 - 14 and 15 - 17 were 42.2 ± 6.9, 42.8 ± 8.4, 42.1 ± 9.1, 46.4 ± 9.2 and 49.7 ± 8.4(P0.05), the neglect rates were 28.0% (326/1163), 28.8% (431/1496), 27.2% (543/1962), 22.4% (373/1664) and 32.8% (563/1716) (P0.05), respectively. There were differences in six neglect types for each group; the neglect degrees and rates were high in the group aged 12 - 14 and 15 - 17 (46.4 ± 9.2 and 49.1 ± 8.4, 22.4% (373/1664) and 32.8% (563/1716), respectively); for each neglect type, the neglect degree of children aged 15 - 17 were highest (52.8 ± 8.0, 47.3 ± 11.6, 49.5 ± 10.8, 42.4 ± 10.3, 52.2 ± 16.0, 56.0 ± 10.1). The degree and rate of neglect in West were highest, Middle was next, the East was lowest (the neglect degrees were 45.4 ± 9.1, 45.0 ± 9.3 and 44.0 ± 8.8, P0.05;the rates were 30.7% (1340/4361), 25.0% (756/3024) and 21.2% (131/616), P0.05). Degree and rate of child neglect for children without siblings were lower than children with siblings (the neglect degrees were 44.2 ± 9.0 and 47.6 ± 9.1, P0.01; the rates were 26.1% (1572/6017) and 33.0% (655/1984), P0.01). Neglect degree of school children aged 6 years old (43.1 ± 7.3) was higher than children not in school (40.7 ± 7.8) (P0.01), but neglect rate was lower (the rates were 35.4% (60/169) and 21.3% (84/394), P0.01).Neglect degree and rate of urban children and adolescents aged 3 - 17 years in China were both high, and neglect deserved more attentions.

To evaluate the predictors and reasons for readmission into cardiac intensive care unit (ICU).A total of 4978 patients underwent cardiac surgery between January 2008 and August 2010. The perioperative risk factors for readmission were analyzed by multivariate regression. And the reasons, outcomes and therapy were analyzed.Among them, 139 patients required ICU readmission. There were 80 males and 59 females with a mean age of 50.3 years (range: 9 - 78). Their median length of first and second stays were 2.00 (1.00 - 4.00) and 3.00 (1.00 - 5.00) days respectively. The median interval from ICU discharge to ICU readmission was 3 (2.00 - 6.75) days and the median hospital stay 24.00 (16.00 - 41.25) days. Readmitted patients had a higher mortality rate than those requiring no readmission (9.4% vs 0.4%, P0.01). The major reasons for readmission were respiratory (n = 69, 49.6%) and circulatory complications (n = 33, 23.7%). Multivariate analysis showed that NYHA (New York Heart Association) classification (95%CI: 1.091 - 3.176, P = 0.023) and the length of initial ICU stay (95%CI: 1.105 - 1.251, P0.01) were independent risk factors of readmission.NYHA classification and the length of first ICU stay are independent risk factors of readmission. Respiratory complications are the most common reasons for readmission.

Melanoma cell adhesion molecule (MCAM) is a cell adhesion molecule that is abnormally expressed in a variety of tumours and is closely associated with tumour metastasis. The role of MCAM in ovarian cancer development has not been fully studied. In this study, through immunohistochemical staining of ovarian cancer tissue samples and RNA interference to silence MCAM in ovarian cancer cells, we examined the impact of MCAM on the biological functions of ovarian cancer cells and attempted to reveal the role of MCAM in ovarian cancer development. Our results showed that MCAM expression was particularly high in metastatic ovarian cancers compared with other pathological types of ovarian epithelial tissues. After MCAM silencing in the MCAM high-expression ovarian cancer cell line SKOV-3, the cell apoptosis was increased, whereas the cell spreading and invasion were significantly reduced, which may be related with dysregulation of small RhoGTPase (RhoA and Cdc42).These results suggest that MCAM expression in ovarian cancer is highly correlated with the metastatic potential of the cancer. MCAM is likely to participate in the regulation of the Rho signalling pathway to protect ovarian cancer cells from apoptosis and promote their malignant invasion and metastasis. Therefore, MCAM can be used not only as a molecular marker to determine the prognosis of ovarian cancer but also as a therapeutic target in metastatic ovarian cancer.

Staphylococcus aureus is an important human pathogen that is renowned both for its rapid transmission within hospitals and the community, and for the formation of antibiotic resistant biofilms on medical implants. Recently, it was shown that S. aureus is able to spread over wet surfaces. This motility phenomenon is promoted by the surfactant properties of secreted phenol-soluble modulins (PSMs), which are also known to inhibit biofilm formation. The aim of the present studies was to determine whether any cell surface-associated S. aureus proteins have an impact on colony spreading. To this end, we analyzed the spreading capabilities of strains lacking non-essential components of the protein export and sorting machinery. Interestingly, our analyses reveal that the absence of sortase A (SrtA) causes a hyper-spreading phenotype. SrtA is responsible for covalent anchoring of various proteins to the staphylococcal cell wall. Accordingly, we show that the hyper-spreading phenotype of srtA mutant cells is an indirect effect that relates to the sortase substrates FnbpA, FnbpB, ClfA and ClfB. These surface-exposed staphylococcal proteins are known to promote biofilm formation, and cell-cell interactions. The hyper-spreading phenotype of srtA mutant staphylococcal cells was subsequently validated in Staphylococcus epidermidis. We conclude that cell wall-associated factors that promote a sessile lifestyle of S. aureus and S. epidermidis antagonize the colony spreading motility of these bacteria.

In the field of tissue engineering, the development of novel switchable cell growth scaffolds and triggered substrate surfaces is desirable for manipulating detachment of cells. In this paper, two kinds of pH-responsive C2-cyclohexane based cell scaffold biomaterials (G1 and G2) have been designed and synthesized. The highlight is that they can induce detachment of cells from material's surface by slightly reducing the pH of culture medium in an acceptable range. The abilities to culture cells on hydrogel scaffolds and guide cells to detach without proteolytic enzyme treatment are very useful for their development in various biomedical applications.

The purpose of this study is to determine how to disclose bad news to patients with cancer in China.One hundred fifty pairs of hospitalized patients and their family members were investigated using a self-designed questionnaire.More patients than their families believed that patients should be informed of their illnesses (98.0% vs. 66.7%, p 0.001), that patients should be informed of their condition completely (69.3% vs. 18.7%, p 0.001), that patients should be informed as soon as the diagnoses were confirmed (49.3% vs. 14.7%, p 0.001), and that patients should be informed by doctors (55.3% vs. 10.7%, p 0.001). κ coefficients between patients and their families on "whether, when and who to disclose" ranged from -0.084 to 0.004. Univariate logistic analyses demonstrated that farmer patients and patients with lower education and lower income were less likely to prefer to be informed completely; farmer patients and patients without an intended curative operation history were less likely to prefer to be informed immediately and directly by doctors. Multivariate analyses showed that farmer patients were less likely to prefer to be informed completely, immediately, and directly by doctors.There was poor or slight concordance in disclosure preferences between patients with cancer and their families. More patients than their families wanted to be informed completely, immediately, and directly by doctors. Farmer patients with cancer were less likely to prefer to be informed completely, immediately, and directly by doctors.

Some in vitro studies have identified an antithrombotic effect of polysaccharides from Laminaria japonica, but this activity remains to be confirmed in vivo. In this study a polysaccharide fraction termed PLG was extracted from L. japonica in the Beibu Gulf in Guangxi, China, and its antithrombotic effects explored in rat models of carotid and venous thrombosis. Its anticoagulation and antiplatelet properties were assessed by measuring the prothrombin time (PT), activated partial thromboplastin time (APTT) and ADP-induced platelet aggregation rate (Agg(max)). Its effects on bleeding time were measured using the tail transection method. It was found that pretreatment with an intraperitoneal injection of PLG at 2.5 or 5.0 mg/kg significantly prolonged the occlusion time in the carotid thrombosis model, and a dose of 5.0 mg/kg reduced the thrombus weight in the venous thrombosis model. Pretreatment with PLG (5.0 mg/kg) increased the APTT and decreased the ADP-induced platelet Agg(max). Neither dose of PLG significantly prolonged the bleeding time compared with the control group. In an in vitro anticoagulation assay using human plasma, PLG at 57.14, 28.57 and 28.57 μg/mL inhibited APTT and PT in a concentration-dependent manner. The results show that PLG possesses antithrombotic activity in a rat model, and that it may prove to be clinically useful in humans.