The vessels’ basement membrane is positive for PAS staining (pink

The vessels’ basement membrane is positive for PAS staining (pink) (original magnification: ×400). Characteristics and follow up of patients Among the 203 patients, there were 154 men (75.86%) and 49 women (24.14%). The mean age at diagnosis was 66 years, ranging from 32 to 77 years. 166 (81.77%) cases reported history of tobacco use, and 37 (18.23%) A-1155463 cases without. 91 (44.83%) cases indicated history of alcohol consumption

and 112 (55.17%) cases without. Patients with tumors located at super glottic were 93 (45.81%) cases, at glottic were 93 (45.81%) cases, and at subglottic were 17 (8.37%) cases. Patients in pTNM stage I, II, III and IV were 25 (12.32%), 60 (29.56%), 62 (30.54%) and 56 (27.59%), respectively. Patients in different T classification T1, T2, T3 and T4 were 27 (13.30%), 93(45.81%), Epigenetics inhibitor 44(21.67%) and 39(19.21%), respectively.151(74.38%) patients showed lymph node metastasis at diagnosis, and 19 (9.36%) patients appeared to show distant metastasis postoperative. In addition, histological grade 1 was in 30 (14.78%), grade 2 was in 149 (73.40%) and grade 3 was in 24 (11.82%) cases. The mean follow-up time was 80 months (range 2-219 months). 121 patients (59.61%) were alive when the follow up ended. Eighty-two patients (40.39%) died as a result of their malignancy. The median

DFS was 56 months. Local recurrence and local lymph node metastasis was observed in 157 patients (77.34%). The mean period from initial surgery to the first local recurrence or metastasis was 63.71 months (range 1-213 months). Nineteen (9.36%) patients developed distant metastasis. The metastatic sites included lung

see more (n = 9), bone (n = 4), liver (n = 3), mediastinum (n = 2), and multiple concomitant metastasis (n = 1, including thoracic this website vertebrae, spinal cord and tibia). Clinical significance of VM in LSCC patients compared with EDV Clinical significance of VM and EDV are listed in Table 1. The positive rate of VM was significantly higher in progressive stage (III and IV) than primary stage (I and II) (27.97% vs. 12.94%) (p = 0.010) clinically, and it was significantly greater in patients with local lymph node metastases than those without local lymph node metastasis (36.53% vs. 16.56%) (p = 0.003). In addition, the positive rate of VM became higher with the raise of histopathological grade: grade 1(6.67%), grade 2 (20.13%), grade 3 (50.00%) (p < 0.0001). And the incidence of VM did not differ with respect to the patients' gender, age, tumor size, T stage, tumor location, recurrence or distant metastasis (all P > 0.05). Table 1 Comparing clinicalpathologic significance of VM and EDV factor   VM     MVD       + – χ 2 P ( ± S) F/t* P Gender     0.881 0.380   1.228* 0.269    M 34 118     17.8739 ± 6.82709        F 10 42     16.6340 ± 6.08995     Age     0.370 0.712   0.108* 0.742    ≥60 22 85     17.4393 ± 6.92216        <60 22 74     17.7514 ± 6.

Serum insulin was increased in both groups

It is evident

Serum insulin was increased in both groups.

It is evident as to why insulin increased in the CHO group as 10 g of carbohydrate were ingested. In addition, the WP group also underwent a similar increase in insulin in the absence of ingested carbohydrate, which is in agreement with the insulin response previously demonstrated with 20 g of whey protein (10 g EAAs) [49]. The Akt/mTOR signalling pathway is activated by insulin. Insulin binds with its receptor and leads to an increase in tyrosine phosphorylation of IRS-1 and eventually mTOR activation. In the present study, 17-AAG order insulin significantly increased in both groups 30 min post-supplement ingestion and 15 min post-exercise, which see more was mirrored by significant MAPK inhibitor increases in IRS-1 activation at 15 min post-exercise. Even though Akt phosphorylation was not significantly increased, activation of IRS-1 likely contributed to the observed increases in mTOR

activation; however, this activity was not preferentially contingent on 10 g of whey protein ingestion. mTOR is a 289 kDa serine/threonine kinase downstream of Akt and stimulates protein synthesis through downstream activation of p70S6K and 4E-BP1, providing a key point of convergence for both resistance exercise and amino acids [14]. Amino acid ingestion has been shown to significantly enhance mTOR signalling [25, 50]. In the present study, the acute bouts of resistance exercise significantly increased mTOR about and p70S6K activation at 15 min post-exercise, while a marked decrease in 4E-BP1 activation was also observed at 15 min post-exercise. While we observed mTOR activation to be enhanced by resistance exercise, the Akt/mTOR pathway signalling intermediates we assessed were unaffected by the provision of 10 g of whey protein comprised of 5.25 g EAAs. Previous work has suggested that a minimal amount of 20 g is needed to stimulate MPS [10]; however, others have demonstrated positive effects utilizing a dosage as low as 6 g EAAs [51].

Increases in MPS following resistance exercise have been observed when utilizing 10 g of whey protein; however, the protein supplement was co-ingested with 21 g of carbohydrate [26]. However, it has recently been shown that approximately 5 g (2.2 g EAAs) and 10 g (4.2 g EAAs) of whey protein without carbohydrate significantly increased MPS 37% and 56%, respectively, over baseline. In this study, it was also shown that 20 g (8.6 g EAAs) maximally stimulated MPS following resistance exercise [27]. Although, our results are supported by previous data which demonstrated that 20 g of albumin protein (8.6 g EAAs) enhanced MPS after resistance exercise, yet had no effects on activation of the mTOR pathway intermediates, S6K1, rps6, and eIF2Bε post-exercise [27], the dosage used in the current study (10 g whey protein, 5.

AMF treatments of MNPs and MNP-loaded cells were performed at 37°

AMF treatments of MNPs and MNP-loaded cells were performed at 37°C in airtight conditions. The temperature of cell pellet was recorded by the infrared thermometer (OS 3708; Omega Engineering,

Stamford, CT, USA). Cell viability assay: MTT assay and trypan blue assay MTT assay Cell viability was measured using 3-(4,PHA-848125 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT; Sigma-Aldrich Company selleck chemicals llc Ltd., Gillingham, Dorset, UK) assay. After being treated in AMF, HeLa cells were reseeded into 96-well petriplate for 2 h incubation in quintuplicate. Following incubation, 20 μL MTT (5 mg/mL in PBS) solution was added to each well and incubated for another 4 h. After that, the culture supernatant was extracted, and purple insoluble MTT product was re-dissolved in 150 μL dimethyl sulfoxide. Lastly, the concentration of the reduced MTT in each well was measured at 570 nm using a microplate

reader. It is notable that the untreated MNP-loaded cells (i.e., the 0 min group) were used as control and absorbance OICR-9429 nmr was adjusted by correcting for the bias caused by the dark MNPs. Trypan blue assay After being treated with AMF, the medium was removed and the cells were stained by 0.4% trypan blue (Sigma-Aldrich Company Ltd., Gillingham, Dorset, UK) solution for 3 min. The cells with damaged cell membranes were stained by trypan blue and counted under the optical microscope. The above tests were repeated three times. Optical images of cellular semi-thin sections, SEM of cell surface, and TEM of cellular ultramicrocuts The HeLa cells were firstly fixed by adding 0.5% and 2% (w/v) glutaraldehyde and kept for 1 h Cell Penetrating Peptide at room temperature. Then the cells were dehydrated with ethanol in

series of concentrations 50%, 70%, 80%, 90%, and 100% (v/v) for 10 min respectively. Finally, the acetone-infiltrated cells were embedded in resin, and the blocks containing the cells were cut into thin sections in 500 or 50 nm using a diamond knife. For TEM of internal cell structure, the 50-nm ultramicrocuts were transferred into a copper grid for viewing. For optical macroscope viewing (6XB-PC, Shanghai Optical Instrument Factory, Shanghai, China), the 500-nm semi-thin sections were observed. For scanning electron microscope (SEM; LEO1530VP; LEO Elektronenmikroskopie GmbH, Oberkochen, Germany) of cell surfaces, the dehydrated cells were conductively coated and observed at 5 kV. Results and discussion Materials characterization TEM images of MNPs (Figure 2) revealed that most spherical MNPs were of a diameter of 200 ± 50 nm, while minority of MNPs was smaller. For rod-shaped MNPs, length was 200 ± 50 nm and diameters ranged from 50 to 120 nm. XRD patterns revealed that both types of MNPs were pure Fe3O4 (JCPDS no 19-0629). Meanwhile, the relatively strong (311) peak of rod-shaped MNPs implied that the crystals grow along the (311) crystallization plane to form rods. The saturation magnetic inductions for the MNPs were similar: 70.

CT scan allows detection and classification of hepatic lesions an

CT scan allows detection and classification of hepatic lesions and excludes the presence of associated injuries; especially injuries BMS202 cost to hollow viscera, although in some cases it underestimates the findings. CT scan, due to its high sensitivity, specificity and accuracy, is an important screening and diagnostic tool for intra-abdominal injuries in hemodynamically

stable patients; patients with altered level of consciousness; and those with difficult clinical examination or associated selleck chemicals pelvic fractures [9–12]. The goal of this study was to determine the effectiveness of nonoperative management of grade IV liver injuries evaluating failure rates; need for angioembolization and blood transfusions; and in-hospital morbidity

and mortality. Methods Our University teaching hospital is one of the referral trauma centers in a metropolitan area of approximately 2.8 million people. This study included patients admitted to our trauma center from 1996 through 2011. The study protocol was reviewed and approved by our institution’s research AZD3965 manufacturer ethics board. Patients were eligible for this analysis if they were adult (15 years or more); sustained grade IV hepatic injury, classified according to the American Association for the Surgery of Trauma Organ Injury Scale (grade IV hepatic trauma corresponds to parenchymal disruption involving 25–75% of hepatic lobe or 1–3 Coinaud’s segments in a single lobe) [1]; and were initially managed nonoperatively as per our hospital guidelines for hepatic injury. We excluded all patients who did MRIP not meet the aforementioned inclusion

criteria. All patients were initially resuscitated in accordance to the Advanced Trauma Life Support (ATLS®) and were submitted to CT scan examination. Selection criteria for nonoperative liver injuries management were hemodynamic stability after initial resuscitation with crystalloid and no need for blood transfusion, absence of clinical signs of peritonitis, and no bowel injuries shown on CT scan. The nonoperative treatment protocol adopted in our trauma division is described in Table 1. Table 1 Protocol of nonoperative management in AAST-OIS grade IV blunt hepatic trauma. Protocol of nonoperative management in AAST-OIS grade IV blunt hepatic trauma – Division of Trauma Surgery – University of Campinas Criteria for patient selection: 1- Abdominal blunt trauma 2- Hemodynamic stability after initial resuscitation with no need for blood: a. Systemic blood pressure > 90 mmHg b. Initial hemoglobin level > 8 3- Evaluation by Computed Tomography with: a. Absence of associated injuries on hollow viscus and pneumoperitonium b.

Lmo-InlA-mur-lux infected A/J mice displayed high IFN-γ levels (Figure 5F) whereas C57BL/6J mice showed low serum concentrations for all of these cytokines and the CCL2 chemokine (Figure 5E-H). Thus, the elevated susceptibility of C3HeB/FeJ mice and their inability to control Listeria replication correlated with an exaggerated production of pro-inflammatory mediators. Serum levels of IL-10 were also high in

Lmo-InlA-mur-lux infected C3HeB/FeJ mice (data not shown). However, this apparently did not result in downregulation of pro-inflammatory responses. Figure 5 Chemokine and cytokine Epigenetics inhibitor production of different mouse inbred selleck kinase inhibitor strains after oral infection with Lmo-EGD-lux and Lmo-InlA-mur-lux. Female C3HeB/FeJ (A), A/J OlaHsd (B), BALB/cJ (C) and C57BL/6J mice (D) were orally infected with 5 × 109 CFU Lmo-EGD-lux or Lmo-InlA-mur-lux. Blood samples were collected at 3 and 5 d.p.i. and cytokine and chemokine levels were determined using Luminex bead assays. 3d and 5d indicate Lmo-EGD-lux infected animals at 3 and 5 d.p.i., respectively; 3d mur and 5d mur indicate Lmo-InlA-mur-lux infected animals at these timepoints (n = 8). For each timepoint, chemokine and cytokine concentrations were determined in triplicate for each inbred mouse and L. monocytogenes strain. Data represent means

± SEM. (E-H) Comparison of chemokine and cytokine production across Lmo-InlA-mur-lux infected mice from the different inbred mouse strains at 5 d.p.i.. Shown are statistical significant differences of indicated cytokine and chemokine levels in the peripheral blood between groups of mice of the analysed inbred mouse strains. Data represent means ± SEM; *p < 0.05, non-parametric Mann–Whitney-U-test. One out of two representative experiments Loperamide is shown (A-H). Oral infection with murinised Lmo-InlA-mur-lux is associated with increased induction of interferon-β An important factor which determines the virulence of Listeria monocytogenes is

the amount of type I interferons produced in the host during infection. High levels of interferon-β (IFN-β) have been demonstrated to be associated with host susceptibility to Listeria infection and mice deficient for IFN-β signalling components such as the type I interferon receptor (Ifnar) gene or the interferon regulatory factor 3 (Irf3) gene are more resistant to lethal L. monocytogenes infection [20–25]. Furthermore, variations in the induction of IFN-β responses in the host by different Listeria strains have been linked with differences in strain virulence [26–29]. To analyse and compare kinetics of Ifnb1 induction after intragastric infection challenge with Lmo-InlA-mur-lux and Lmo-EGD-lux we developed a dual luciferase detection model.

7 h and 56 6 mL/min, respectively This study utilized an ultrafi

7 h and 56.6 mL/min, respectively. This study utilized an ultrafiltration rate of 2 L/h and a dialysate rate of 1–2 L/h. In contrast to the studies listed above, other studies have found considerably lower clearance see more rates than our study. Armendariz and colleagues presented a case report of a patient undergoing CVVH and found that total body clearance of amikacin was 10.5 mL/min and CVVH clearance was 10.11 mL/min [15]. This approximated the hemofiltration rate to be 10 mL/min. They found an elimination constant of 0.023 h−1, which corresponds to a t ½ of 29.7 h. This study found clearance rates from CRRT to be similar to those reported for patients

in renal failure without the use of dialysis. The median clearance rate of amikacin in our study (36.7 mL/min) was drastically higher than that reported by Armendariz and colleagues. Of note, the dialysate flow rates described in the current report are approximately twice those reported by Armendariz and colleagues [15]. Given the high sieving coefficient of 0.93 for amikacin, it is conceivable that the flow rates during CRRT would dictate the amount of drug removal [26]. This premise is supported by other studies that utilized higher dialysate or ultrafiltration rates with subsequent findings 8-Bromo-cAMP purchase of higher rates of amikacin clearance. Roberts and

colleagues reported data from five patients on CVVH, with average flow rates of 19.2 mL/min (1.2 L/h) and found through a mean hemofiltration clearance rate of 16.4 mL/min [18]. Taken together, it appears that across studies, the overall dialytic dose may affect amikacin clearance. This is consistent with the findings of our current study, which suggest that dialytic dose correlates with amikacin clearance. However, there are still many other factors that would ultimately determine the PK BAY 63-2521 mouse profile of amikacin. These may include inter-patient variability in non-dialytic measures, such as volume status, non-renal intrinsic clearance, the age of the filter, and interruptions to CVVHD. Of interest, a study by Cotera and colleagues that evaluated amikacin clearance

in five patients with acute oliguric renal failure undergoing CVVHD found that the amikacin clearance rates were only 3.57 and 4.18 mL/min with 1 and 2 L/h dialysate rates, respectively [16]. Even though the 2 L/h dialysate rate was only slightly lower than that reported in the current study, the authors noted drastically lower clearance rates than in our study. This could potentially be explained by the type of hemodialyzer membrane utilized. Notably, all the previous studies discussed and the current study utilized synthetic hemodialyzer membranes composed of either acrylonitrile or polysulfone. In contrast, the study by Cotera and colleagues [16] utilized a cuprofen (cellulose) dialysis membrane. A decrease in drug clearance with the use of cellulose dialysis membranes compared to polysulfone has been well documented [27–30].

Lopes Bezerra L, Filler S: Interactions of Aspergillus fumigatus

Lopes Bezerra L, Filler S: Interactions of Aspergillus fumigatus with endothelial cells:internalization, injury, and stimulation of tissue factor activity. Blood 2004, 103:2143–2149.CrossRefPubMed 45. Mehrad B, Strieter RM, Standiford TJ: Role of TNF-alpha in pulmonary host defense

in murine invasive aspergillosis. J Immunol 1999, 162:1633–40.PubMed 46. Netea MG, Warris A, Meer JW, Fenton MJ, Verver-Janssen TJ, Jacobs LE, Andresen T, Verweij PE, Kullberg BJ: Aspergillus fumigatus evades immune recognition during germination through loss of toll-like receptor-4-mediated signal transduction. J Infect Dis 2003, 188:320–6.CrossRefPubMed 47. Behnsen J, Hartmann A, Schmaler J, Gehrke A, Brakhage A, Zipfel PF: The opportunistic human pathogenic

fungus Aspergillus fumigatus evades the host complement Ulixertinib system. Infect Immun 2008,76(2):820–827.CrossRefPubMed 48. Lieber M, Smith B, Szakal A, Nelson-Rees CH5183284 W, Todaro S: A continuous tumor-cell line from a human lung carcinoma with properties of type II alveolar epithelial cells. Int J Cancer 1976, 17:62–67.CrossRefPubMed 49. Cozens AL, Yezzi MJ, Kunzelmann K, Ohrui T, Chin L, Eng K, Finkbeiner WE, Widdicombe JH, Gruenert DC: CFTR expression and chloride secretion in polarized immortal human bronchial epithelial cells. Am J Respir Cell Mol Biol 1994,10(1):38–47.PubMed 50. Million K, Tournier F, Houcine O, Ancian P, Reichert U, Marano F: Effects of retinoic acid receptor-selective agonists on human nasal epithelial cell differentiation. Am J Respir Cell Mol Biol 2002,25(6):744–750. 51. Morigi M, Zoja C, Colleoni S, Angioletti S, Imberti B, Donadelli R, Remizzi A: Xenogeneic

Serum Promotes Morin Hydrate Leukocyte-Endothelium Interaction under Flow through Two Temporally Distinct Pathways: role of complement and nuclear factor-kappaB. J Am Soc Nephrol 1999, 10:2197–2203.PubMed 52. Griese M, Reinhardt D: Smaller sized particles are preferentially taken up by alveolar type II pneumocytes. J Drug check details Target 1998, 5:471–479.CrossRefPubMed 53. Krisanaprakornkit S, Chotjumlong P, Kongtawelert P, Reutrakul V: Involvement of phospholipase D in regulating expression of anti-microbial peptide human beta-defensin-2. Int Immunol 2008,20(1):21–29.CrossRefPubMed 54. Pfaffl MW: A new mathematical model for relative quantification in real-time RT-PCR. Nucleic Acids Res 2001,29(9):e45.CrossRefPubMed 55. Livak KJ, Schmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)). Methods 2001, 25:402–408.CrossRefPubMed 56. Hahn CL, Best AM, Tew JG: Rapid tissue factor induction by oral streptococci and monocyte-IL-1beta. J Dent Res 2007,86(3):255–259.CrossRefPubMed 57. Jang BC, Lim KJ, Choi IH, Suh MH, Park JG, Mun KC, Bae JH, Shin DH, Suh SI: Triptolide suppresses interleukin-1beta-induced human beta-defensin-2 mRNA expression through inhibition of transcriptional activation of NF-kappaB in A549 cells. Int J Mol Med 2007,19(5):757–763.PubMed 58.

More importantly, we proved that ANKRD12 expression was significa

More importantly, we proved that ANKRD12 expression was significantly associated with overall survival of CRC patients. In support of this, Kaplan–Meier analysis of overall survival showed that patients whose tumors had lower ANKRD12 expression tend to have a significantly worse overall survival, indicating that low ANKRD12 level is a marker of poor prognosis for CRC patients. Moreover, Cox proportional hazards model showed that low ANKRD12 expression

was an independent prognostic predictor for CRC patients. Therefore, ANKRD12 could constitute a molecular prognostic RGFP966 solubility dmso marker for CRC patients, identifying who are more likely to have higher risk of death and need receive a more aggressive treatment. The precise molecular mechanisms behind the altered expression of ANKRD12 in colorectal cancer are unclear. To our knowledge, this is the first report to describe the significance of ANKRD12 to clinical stage, lymph node and liver metastases, and prognosis of CRC patients. ANKRD12 binds to alteration/deficiency in activation 3(ADA3)

through its C-terminal domain and inhibits ADA3-mediated transcriptional co-activation on NRs [7]. ADA3 is a component of the human P/CAF acetyltransferase complex which is thought to link co-activators to histone acetylation and basal transcription machinery [14]. Gene expression regulated by NRs, therefore ANKRD12 may regulate some important gene expression by inhibiting ADA3-mediated transcriptional co-activation on NRs. Recently, ADA3 is also identified Anidulafungin (LY303366) as APR-246 supplier a p53-binding protein [15–17], as well as causing p53 acetylation [18]. In mammalian cells, overexpression of ADA3 increased p53 levels [16]. P53 was identified as a tumor suppressor protein and is the most commonly mutated gene in human cancers [19–21]. However, ANKRD12 has little or no effect to promote p53 activation [7]. So we speculated that the effects of ANKRD12 in tumor development or progression might, through binding to ADA3 co-activators, increasing p53 levels and inhibit tumor development or progression. Additional Selleckchem Alpelisib studies

to investigate the real molecular mechanisms of altered expression of ANKRD12 in the development or progression of CRC are essential. Conclusions In conclusion, we found that ANKRD12 mRNA were downregulated in CRC tumor tissues and low ANKRD12 mRNA expression correlated with poor overall survival and liver metastasis of CRC patients. These findings suggest that ANKRD12 is a cancer-related gene associated with liver metastasis and a survival predictor of CRC patients. Consent Written informed consent was obtained from the patient for publication of this report and any accompanying images. Acknowledgements We thank Jun Ye, Hai Liu, Zhixuan Fu and Zhigang Chen for their technical assistance and the entire laboratory for fruitful discussions.

As for CH-C1 xerogel from 1,4-dioxane, due to the flexibility of

As for CH-C1 xerogel from 1,4-dioxane, due to the flexibility of ether band in the molecular skeleton and different intermolecular forces with solvents, after the intermolecular hydrogen bonding and orderly

stacking in different solvents, various repeating units with different lengths were obtained. So selleckchem corresponding d values of 4.07 and 2.84 nm were obtained from 1,4-dioxane and nitrobenzene, respectively, as shown in Figure  7a,b. As for CH-C3 with an additional diphenyl group linked by ether band in the spacer part, the combination of a flexible ether band and a rigid diphenyl segment in the molecular spacer with π-π stacking seemed more suitable to adjust molecular conformation to self-assemble and form organized stacking nanostructures. The obtained experimental value of CH-C3 in nitrobenzene was 2.14 nm, which was near half of the calculated molecular length, suggesting a symmetrical stacking mode, shown in Figure  7c. In addition, for the case of CH-C4 with a five-carbon alkyl substituent chain linked by phenoxy ether band in the molecular spacer, due to the addition of a flexible

alkyl segment and a weak hydrophobic force between alkyl chains, it can also stack and form some belt-like aggregates with a stacking length of 3.23 nm in nitrobenzene, as shown in Figure  7d. Moreover, for CH-C2 and CH-N1, the inefficient or poor gelation behaviors in the present solvents

may be mainly attributed to the too rigid or too flexible spacers in molecular skeletons, which cannot cause enough intermolecular forces to make the molecules align and stack in an organized way to form various nanostructures. Meanwhile, it should be noted that this phenomenon can be compared with the results of our recent works [24, 25, 48]. Therein, functionalized imide derivatives with the substituent groups of cholesteryl, azobenzene, luminol, and benzimidazole/benzothiazole residue can have a profound effect on the gelation abilities and the as-formed nanostructures of the Erastin purchase studied compounds. For the present gelators, the experimental data showed that the spacers in the molecular skeleton have played a crucial role in the gelation behavior of all gelators in various organic solvents. Suitable combination of flexible/rigid segments in molecular spacers in the present cholesteryl gelators is favorable for the gelation of organic solvents. Now, the drug release behaviors generated by the present xerogels in the mixture of Congo red are under investigation to display the relationship between the molecular structures of as-formed nanostructures and their properties. Figure 7 Rational assembly modes of CH- C1, CH- C3, and CH- C4 in gels. Experimental values of (a, b) CH-C1 in 1,4-dioxane and nitrobenzene, (c) CH-C3 in nitrobenzene, and (d) CH-C4 in nitrobenzene.

To test the performance of the field emission and measurement of

To test the performance of the field emission and measurement of current level, during the experiment,

the two MWCNT vacuum devices, a high vacuum chamber, and the learn more tip-off system were connected to the same vacuum level. MWCNT for the vacuum gauge was packaged by tip-off through a vacuum system at a pressure of 1.3 × 10-6 Torr. The vacuum gauge output was measured by using a source meter (Keithley 2400, Cleveland, OH, USA) and LabVIEW software (National Instruments Corp., Austin, TX, USA). Figure 1 Structure of MWCNT device and FE-SEM image of MWCNT paste after heat treatment. (a) Structure of the MWCNT device. (b) FE-SEM image of MWCNT paste printed on ITO glass substrate after heat treatment. Figure 2 Schematic of the high vacuum chamber with tip-off system. Results and discussion Figure 3a shows the field emission characteristic of printed CNT before and after vacuum packaging. The turn-on field required to reach a current density AICAR mouse of 10 μA/cm2 was 2.54 V/μm (610 V) and 2.5

V/μm (600 V) with tip-off (Sample 1) and vacuum chamber (Sample 2) processes, respectively. Figure 3b shows the Fowler-Nordheim (F-N) plot (ln(I/V 2 ) versus 1/V) and nonlinear slopes. At an applied voltage of 950V, the emission current of MWCNT film decreased from 0.9 to 0.7 mA after the tip-off. The reasons for this could be explained by vacuum level change due to outgassing inside the flat panel during tip-off process. Figure 3 Current versus voltage properties for the printed MWCNT paste film (a). The F-N plots (b). Figure 4 exhibits the plot of the current versus time of the packaged see more device which was loaded in the vacuum chamber tip-off system (Sample 1). In this experiment, applied voltage to the vacuum gauge was 1 V. The measurement of the current was initiated after saturation was reached by the rotary pump and the turbo pump. As the gauge was heated by the tip-off heater from 2,000 to 2,300 s, the current increased after heater was turned on and decreased gradually following the turning-off of the heater. This phenomenon can be probably explained by the fact that there is limit in the amount of outgas that can be removed by the pumps. When the vacuum

status approached many to 1.2 × 10-6 Torr, the device was tipped off. The tip-off process was as follows: glass tip was located on the heater, which was in the vacuum chamber, and heated. The heater made the temperature exceed the melting point of the glass in a few minutes. At this instance, melted glass was held together for a short time to close the glass tip and separated from the vacuum pump. The outgas generated by heating and field emission resulted in the increase of the current, i.e., the current increased upon exposure to field emission outgases. Figure 4 Current changes of the MWCNT device during tip-off process. Figure 5 shows the current of the MWCNT vacuum gauge at the device versus time inside high vacuum chamber (Sample 2).