80% to 23 74%, and the healing rates at 12 h, 24 h and 36 h (p <

80% to 23.74%, and the healing rates at 12 h, 24 h and 36 h (p < 0.001). By 17DMAG cell line contrast, the healing rate of NPC 5-8 F cells was not affected by treatment of lipofectamine alone and transfection of pEGFP-C3 and PinX1-FAM-siRNA (p > 0.05). Figure 6 Effect of PinX1 on wound healing ability of nasopharyngeal carcinoma

5-8 F cells in scratch assay. Cells transfected with pEGFP-C3-PinX1 (a), pEGFP-C3 (b) and PinX1-FAM-siRNA(e), treated with lipofactamine alone (c), and untreated (d) were inoculated in 6-well plates pre-coated with collagen IV, cultured in media containing 10% newborn calf serum till forming monolayer, then scratched and photographed at 0 h, 12 h, 24 h and 36 h after scratching. The results show that overexpression of PinX1 by transfection of pEGFP-C3-PinX1 significantly increased the wound healing time ACY-241 mw of NPC 5-8 F cells, while downregulation of PinX1 by transfection of FAM-siRNA reduced has no effect on wound healing. We then examined the effect of PinX1 on hTERT mRNA level and telomerase activity. As shown in Tables 4 and 5 and CB-5083 molecular weight Figures 7 and 8, overexpression of Pin X1 by transfection of pEGFP-C3-PinX1 significantly reduced hTERT mRNA level by 21% and decreased

telomerase activity in NPC 5-8 F cells (p = 0.000). By contrast, reduced PinX1 by transfection of PinX1-FAM-siRNA had effects on neither hTERT mRNA Farnesyltransferase level nor telomerase activity in NPC 5-8 F cells (p > 0.05). In addition, hTERT mRNA level and telomerase activity in NPC 5-8 F cells were not affected by transfection of pEGFP-C3 and treatment of lipofectamine alone. Table 4 hTERT

mRNA level in each group Sample hTERT mRNA F P pEGFP-C3-PinX1 0.789 ± 0.024* 117.689 0.000 pEGFP-C3 0.978 ± 0.011     Lipofectamine alone 0.987 ± 0.014     Untreated 1.000 ± 0.000     PinX1-FAM-siRNA 1.001 ± 0.085**     * vs untreated, P < 0.001, ** vs untreated, P > 0.05. hTERT mRNA level was normalized to GAPDH. Table 5 Telomerase activity in NPC cells Samples Telomerase activity F P pEGFP-C3-PinX1 36227.63 ± 2181.748* 53.816 0.000 pEGFP-C3 58346.993 ± 2181.748     Lipofectamine alone 59697.199 ± 2181.748     Untreated 62552.354 ± 2181.748     PinX1-FAM-siRNA 63600.608 ± 2181.748**     * vs untreated, P < 0.001; ** vs untreated, P > 0.05. Figure 7 Effects of PinX1 on hTERT mRNA level in NPC 5-8 F cells. PinX1 mRNA levels in NPC 5-8 F cells transfected with (a) pEGFP-C3-PinX1, (b) with pEGFP-C3, (c) treated with lipofectamine alone, (d) untreated and (e) transfected with PinX1-FAM-siRNA were measured in RT-PCR and normalized to internal control GAPDH. Data were presented as mean value of three experiments showing that overexpression of PinX1 significantly decreased hTERT mRNA level. Figure 8 Effect of PinX1 on telomerase activity in nasopharyngeal carcinoma cells.

Note that the fluorous solvent is chemically inert to most organi

Note that the fluorous solvent is chemically inert to most organic and inorganic materials [14, 15]. The patterned TNP layer was annealed at 80°C for 2 h and then at 450°C for 30 min. As shown in Figure 

2a, the TNP pattern whose width (w) and distance (d) were 500 μm, respectively, was well defined according to the PDMS pattern. In principle, the TNP patterns can be achieved down to check details a submicrometer scale depending on the dimension of the elastomer stamp patterns or the SL patterns [11]. Figure 1 selleck products Schematic diagram showing each step of our micropatterning method of TNPs. (a) Transfer printing of the SL on a patterned FTO glass using a PDMS stamp. (b) Doctor-blading TNP paste on the SL-patterned FTO glass to form a TNP layer of 2.5 μm thick.

(c) Soft-curing of the TNP layer at 50°C for 3 min and the lift-off process of the SL. Figure 2 Schematic diagram of TiO 2 pattern, images taken with optical microscopy and FE-SEM, and solid 19   F-NMR spectra. (a) Dimension of a TiO2 pattern: the width (w), the distance (d), and the height (h) are 500, 500, and 2.5 μm, respectively. (b) The optical microscopic image of the TNP patterns on the FTO glass. (c) The FE-SEM PRN1371 in vivo image of the cross section of the patterned TNP layer of 2.5 μm thick. (d) The high-resolution FE-SEM image of the highly packed TNPs. The solid 19 F-NMR spectra of (e) an empty rotor and (f) a TNP layer after being treated with a fluorous solvent. Preparation of a DSSC array Each patterned TNP used GNA12 as an individual photoanode for a unit cell was connected in series for

a high-voltage DSSC array. The patterned TNP layer was immersed in a solution of 3 mM Z907 dye (Solaronix SA) dissolved in a 1:1 mixture of acetonitrile and tert-butyl alcohol for 24 h. The dye-coated TNP layer was simply washed with acetonitrile. For the solid-state hole transport material (HTM), spiro-OMeTAD (American Dye Source, Inc., Baie D’Urfé, Quebec, Canada) dissolved in chlorobenzene was mixed with a lithium bis(trifluoromethylsulfonyl)imide salt ionic dopant dissolved in acetonitrile. The solution was placed on the whole TNP-patterned FTO glass, and the pores in the TNP layer were filled with the solution by capillary action for 1 min. The TNP-patterned FTO glass was then spun at the rate of 2,000 rpm. For the preparation of a cathode, Au of 100 nm thick was thermally deposited at the rate of 1 Å/s through a shadow mask to connect 20 cells in series. The array of 20 DSSCs connected in series has a total active area of 1.4 cm2. Characterization methods An optical microscope and a field emission scanning electron microscope (FE-SEM; SU-70, Hitachi, Ltd., Chiyoda, Tokyo, Japan) were used for taking the images of the patterned TNP layer.

There is distention of the gall bladder with abundant luminal acc

There is distention of the gall bladder with abundant luminal accumulations of mucus interspersed with scant amounts of bile. The mucosa of the gall bladder is lined by moderately hyperplastic columnar epithelial cells with accentuation of the normal folds by accumulations of mucus. Within the lamina propria and the tunica muscularis there are occasional multifocal to perivascular accumulations of lymphocytes and rare plasma cells. Hematoxylin

and eosin staining. Bar = 250 μm. Sequencing of Canine ABCB 4 Sequencing of all exons (1 to 26) of canine ABCB4 was performed on genomic DNA from cheek swab samples (Shetland Sheepdogs) or from archived liver tissue (affected dogs that Gamma-secretase inhibitor were not Shetland Sheepdogs). A single base pair insertion (G) was identified in exon 12 (Figure 2) in 14 of 15 affected Shetland Sheepdogs, 1 of 21 unaffected Shetland Sheepdogs, and 3 affected dogs of other breeds (Cairn Terrier, Vadimezan cell line Cocker Spaniel,

and Pomeranian). The insertion mutation (ABCB 4 1583_1584G) is significantly associated (P < 0.0001) with the diagnosis of gallbladder mucocele in Shetland Sheepdogs, with an odds ratio of 280 (95% CI 12.7-12,350). In other dog breeds, ABCB 4 1583_1584G is also significantly associated with the diagnosis of gallbladder mucocele (P < Selleckchem TSA HDAC 0.0006). The frame shift generated by the insertion results in 4 premature stop codons within exon 12. The full canine ABCB 4 gene contains 26 exons which encode essential

structural elements that characterize ABC transporters: two ATP binding domains and two substrate binding sites. Essential structural elements of ABCB4 normally contained within exon 12 and subsequent exons include both ATP binding sites and a substrate binding site. Figure 2 Electropherograms for wildtype and mutant canine ABCB 4. The insertion is indicated by an arrow. A missense mutation in exon 15 of canine ABCB 4 was identified in the one affected Shetland Sheepdog that did not harbor ABCB 4 1583_1584G. This SNP results in a nonhomologous amino acid substitution (alanine to serine) in exon 15 which may affect tertiary protein structure. However, this mutation was also present in 9 of the 21 unaffected Shetland Sheepdogs and 10 of the 15 affected Shetland Sheepdogs, so its significance GABA Receptor is unclear. No obvious differences were apparent in disease severity or biochemical parameters in the affected dogs with the mutation in exon 15. Confirmation of Insertion by Allele Specific PCR To confirm the presence of ABCB 4 1583_1584G as well as determine the genotype of each dog, allele specific primers were designed and used to amplify the region of interest in exon 12 (Figure 3). All dogs harboring the insertion were heterozygous at the mutant allele suggesting a dominant mode of inheritance with incomplete penetrance. None of the dogs in the study were homozygous for the mutant allele. Genotype frequencies are shown in Table 3.

sobrinus using S sobrinus-free saliva and S sobrinus-free denta

sobrinus using S. sobrinus-free Etomoxir solubility dmso saliva and S. sobrinus-free dental plaque as an alternative in the spiking experiment. As shown in Figure 3, neither saliva nor dental plaque inhibited the PCR, indicating that this assay is applicable

for measuring cariogenic bacteria in oral specimens. We next examined the correlation between the numbers of viable S. mutans cells in oral specimens as detected by PMA-qPCR and by culture. We found a positive correlation between these quantification methods for both carious dentin and dental plaque. Compared with culture, the number of viable S. mutans cells was overestimated by PMA-qPCR. It may be that the culture method www.selleckchem.com/products/EX-527.html usually underestimates the cell number. The cell number determined by conventional qPCR correlated with the cell number determined by culture. Several previous investigations have reported that the cell number determined by qPCR correlated with CFU [14, 15]. However, compared with PMA-qPCR, conventional qPCR overestimated the cell number to a greater extent in both types of clinical specimens. Therefore, the cell culture

count was closer to the number determined by PMA-qPCR than to that determined by conventional qPCR in the present study. Monitoring viable bacterial cells in oral specimens provides information to help understand oral infectious diseases. When we compared the total and viable cell numbers in carious dentin from patients with dental caries and dental plaque from caries-free children, there was no significant difference DMXAA between carious dentin and dental plaque in terms of either total number S. mutans cells or number of viable cells. We may not be able to simply compare the cell numbers in these specimens because the contents are not identical. Nevertheless, there was no significant difference in the percentage of viable cells between the specimens. However, there was a significant difference in total cell number and viable cell number between saliva from patients with dental caries and saliva from caries-free children. Monitoring of the viable cell number in relation to the total cell number in oral specimens has not previously

been performed. To understand the variation in the viable cell number, both the viable and total cell numbers must be determined. To further understand Florfenicol cell viability in relation to dental caries, a greater number of specimens should be analyzed. When the relationship between the number of viable S. mutans cells in saliva and in dental plaque from caries-free children was analyzed using PMA-qPCR, a positive correlation was found between viable S. mutans cells in saliva and in dental plaque. This result was consistent with previous reports [16]. There was no significant correlation between the number of viable S. mutans cells in saliva and that in carious dentin from caries patients in the present study. Our data suggest that saliva reflects the number of viable cells in caries-free plaque, but not in carious dentin.

The degrees of its expression were associated with differentiatio

The degrees of its expression were associated with differentiation of tumor, TNM division, peritoneal seeding and vascular invasion check details remarkably. Patients with high expression of SPARC have worse prognosis than those with low expression of SPARC. Taken together, higher SPARC expression was significantly associated with tumour progression and advanced stages of gastric cancer. Recent research of Inoue M et al[23] even identifed SPARC as a candidate target antigen for immunotherapy of various cancers including gastric cancer by genome-wide cDNA microarray. It is exciting that therapy targeting the SPARC subunit may be a useful Selleckchem AG-881 approach to suppress gastric cancer growth. However, the molecular

mechanisms selleck kinase inhibitor responsible for the oncogenesis of SPARC in gastric cancer is not entirely understood. Through expression analysis of a panel of gastric cancer cell lines, we showed that SPARC is also overexpressed in sevel human gastric cancer cell lines. Therefore, we tested our hypotheses that SPARC may be a key molecule in gastric cancer invasion, and that targeting SPARC may present a novel therapeutic strategy for anti-invasion of gastric cancer. Dissemination of cancer cells, either locally or at distant metastatic sites, requires that malignant cells acquire the ability

to invade the basement membrane and to adhere to other matrices. It has been suggested that SPARC may play a key role during the initial steps in the process of tumour invasion and metastasis[24]. In addition, SPARC can induce the expression of metalloproteinases or enzymes that subsequently play an important role in the degradation

of basal membranes and extracellular matrix components[25]. SPARC was associated with the invasiveness of meningiomas[26, 27] and gliomas[28]. Furthermore, suppression of SPARC expression using antisense RNA inhibited motility and invasion of human breast cancer cells in vitro[21]. To determine if SPARC siRNA could reduce protumorigenic cellular behaviors associated with SPARC expression, we first determined the effect of decreased SPARC expression on tumor cell invasion. We measured the capacity N-acetylglucosamine-1-phosphate transferase of gastric cancer cells to invade through Matrigel, an artificial extracellular matrix, after transfection with SPARC siRNA or a non-targeting control siRNA. Decreased SPARC expression led to the inhibition of invasion by 69% and 79% in MGC803 and HGC27, respectively. Thus, SPARC siRNA can decrease gastric cancer invasion in vitro. A recent study found that SPARC protects cells from stress-induced apoptosis in vitro through an interaction with integrin β1 heterodimers that enhance ILK activation and prosurvival activity[28]. Initial studies using antisense RNA strategies completely abrogated human melanoma growth in nude mice[21]. Horie et al.[29] showed that the downregulation of SPARC expression induced growth inhibition with G1 arrest in human melanoma cells.

In addition, the diameter of the Ge/GeO x nanofilaments (or NWs)

In addition, the diameter of the Ge/GeO x nanofilaments (or NWs) of approximately 40 nm is calculated using a new method under SET. The low-current operation of this RRAM device will make it useful in nanoscale nonvolatile memory applications. Methods Ge NWs

were grown by the VLS technique using Ge https://www.selleckchem.com/products/Gefitinib.html powder as the starting material (purity of 99.999%). Silicon (Si) wafers with an ultrathin gold (Au) coating as a catalyst were used as substrates. The substrate was annealed at 600°C for 30 min in a vacuum chamber to form isolated Au nanoparticles (NPs), or commercial Au NPs were used as substrates to grow NWs. The typical diameter of the Au NPs was approximately 5 nm, which was determined by scanning electron microscopy (SEM) (Figure 1a). Ge powder was placed in an alumina selleck boat and inserted in a horizontal tube furnace. The furnace was heated at 900°C for 30 min under argon with a flow rate of 10

sccm to grow NWs through the VLS technique. High-density Ge NWs with a diameter of approximately 100 nm and length of approximately 100 μm were observed by SEM (Figure 1b). The Ge NWs possessed a core-shell structure, find more as shown in the transmission electron microscopy (TEM) image in Figure 1c. This suggests that the core region is Ge-rich, and the shell region is oxygen-rich, i.e., GeO x . It is expected that the GeO x layer will contain more defects than the Ge-rich core, which may be useful for resistive switching memory applications. The defects in the Ge/GeO x NWs were observed by both XPS and PL (Figures 2 and 3). PL measurements were obtained on a Triax 320 monochromator (Jobin Yvon, Edison, NJ, USA) and photomultiplier detector with an excitation wavelength of 325 nm. Figure 1 SEM and TEM images. SEM images of (a) Au nanoparticles and (b) Ge NWs on Si substrates. (c) TEM image of core-shell Ge/GeO x NWs. Figure 2 XPS spectra of Ge 3 d core-level

electrons of the Ge/GeO x NWs. Figure 3 PL and deconvoluted spectra. PL spectra of the Ge/GeO x NWs (a) measured at temperatures of 10 to 300 K and (b) deconvoluted spectra at 300 K. Defects in the Ge/GeO x NWs and resistive switching memory characteristics were also assessed by fabricating an IrO x /Al2O3/Ge NWs/SiO2/Si TCL MOS structure, as shown in Figure 4a. MOS capacitors were fabricated using a shadow mask to pattern IrO x electrodes onto Al2O3 that was grown on dispersed Ge/GeO x NWs. The memory device consisted of three stacked layers: a top tunneling layer of Al2O3 (10 nm), a defect-rich Ge NW layer, and a thin tunneling layer of SiO2 (approximately 4 nm). After cleaning the Si wafer, an SiO2 layer was grown by annealing in a hot furnace as described above. The Ge/GeO x NWs were then dispersed on the SiO2/Si substrate. To deposit the TE of IrO x , a thin layer of Al2O3 was also deposited.

The laboratory ferret (Mustela putorius furo) is not only suscept

The laboratory ferret (Mustela putorius furo) is not only susceptible to human isolates of seasonal, avian and pandemic influenza viruses, but pathogenesis and severity of the respective clinical manifestations

of these infections are to a large extent similar to those found in humans [18, 19]. Therefore, to address the hypothesis that humans at risk for vascular disease may develop clinically overt vascular thrombosis during or shortly after influenza virus infection [20], we collected plasma samples during a time course pathogenesis experiment in which ferrets were infected with seasonal-, avian- or pandemic influenza viruses [21]. Even though ferrets are not generally considered to represent the high risk patients for vascular thrombotic disease, ATM Kinase Inhibitor they do offer a biologically variable and reliable animal model to address the activation of coagulation during influenza virus infection. Prothrombin time, activated partial thromboplastin time, von Willebrand factor

(VWF) activity, D-dimer levels, and thrombin-antithrombin complexes were measured in sequentially collected plasma samples. In addition fibrin staining was carried out on the lungs of infected animals upon euthanasia to address the coagulation status at the tissue level. All these parameters were evaluated in relation to virological parameters and data on disease severity. Results Clinical signs, pathology and virology of ferrets after infection with H3N2-, pH1N1- or highly pathogenic H5N1 Selleckchem Gilteritinib avian – influenza viruses Clinical signs, pathological changes and virological parameters of this time course experiment in ferrets have been reported Calpain previously [21]. Data important for this study are AZD6244 ic50 summarized in Table 1. In

short, clinical signs varied greatly between the three influenza virus and mock infected groups. All animals infected with H3N2, pH1N1, or mock infection, survived the infections. H3N2 virus infected ferrets showed mild clinical signs; nasal discharge, sneezing, decreased tendency to eat, and bodyweight decrease by 11% (SD 8.5-13%) at 7 dpi. Detection of infectious virus was restricted to the nose and peaked at 1 dpi. Upon necropsy the lungs of the H3N2 infected ferrets showed up to 10% consolidation by gross pathology while the relative lung weights did not differ from the controls. Table 1 Overview of the clinical data (bodyweight decrease, relative lung weight, lung damage) and virological parameters (virus titers) partly adapted from Van den Brand et al. 2012 Plos One[21] Day   1 2 3 4 7 14 Bodyweight H3N2 -51 -100 -69 -124 -186 -205 (16–86) (9–190) (33–104) (117–130) (141–231) (101–309) pH1N1 -68 -169 -142 -250 -251 -193 (22–114) (161–176) (74–210) (185–315) (190–312) (19–368) H5N1 -70 -131 -170 -190 ┼ ┼ (35–105) (112–149) (142–198) (135–246)     Control -44 -20 +7 -34 -62 -46 (31–57) (+30 – -69) (+40- -25) (+19 – -88) (+10 – -134) (+30 – 123) Relative lung weight 10-2 gram H3N2 0.6 0.6 0.6 0.6 0.6 0.6 (0.5-0.7) (0.6-0.

In this work, we study the case, in which the distances between a

In this work, we study the case, in which the distances between atoms are quite large, so that the average distances between atoms are greater or in the same order than the

‘resonant transition’ wavelength. Therefore, we prepare an ensemble of N two-level atoms initially in ground state, SGC-CBP30 in vitro and a single mode of the radiation field is excited in a ‘Fock’ state (so called one-photon state). This is the case of a purely monochromatic wave with zero line width under the consideration. A laser output in single mode operation can approximate this situation due to its high degree of monochromaticity (small line width) for instance. The mode of electromagnetic field is specified completely by giving its wave vectors k 0 with atomic learn more transition frequency ω = c|k 0| and its polarization j (j = 1, 2). The main feature, differentiating our research from others in this domain, is the developed direct and consistent solution to the N-particle equations, describing the time evolution of the N atomic probability state amplitudes. Besides, in certain sense, we explained the nature of the widely used Weisskopf-Wigner approximation that was not found in the reviewed by us scientific

literature. The goal of this paper can be formulated as an attempt to propose an adapted and simple in practical use theory, for example in the highly applied nanoscale physics. The proposed theoretical material requires corresponding Belinostat concentration experimental verification. As an idea of an application, the model system can be realized on atomic (developing the method proposed in [1] for the nuclei of 57Fe in certain composites, but this time for a visible region), chains of trapped ions (like in [8]), and molecular structures for further developing such techniques like FRET (described for instance in [12]), atomic chains like carbyne loops (for example, [13]), and microhole array synthesized by femtosecond laser radiation (see [14], for an instance). Let us first provide below some general theoretical premises. More detailed derivations of the corresponding

mathematical model Methane monooxygenase can be found in [11]. Methods The equations of motion for the state amplitudes We have assumed that the atomic energy levels have no linewidth, so that, only if , the atoms can be able to absorb a photon. Obviously, this is an unrealistic case since it is impossible to have a completely monochromatic wave. In addition, for the case of the Fock initial state, in which we measured the energy precisely of the mode, the average electric field will be zero. In the forth of the law of energy conservation, an emitted photon will correspond to the same frequency (we can say it will occur with a high probability after a quite long time interval if the system has a damping). Therefore, consider a collection of N identical atoms, at positions r 1,…,r α ,…,r N , coupled to a one mode electromagnetic (EM) field. Each atom α = 1..

The cells were treated with 10 ng/ml of recombinant human TNF-α (

The cells were treated with 10 ng/ml of recombinant human TNF-α (Wako) for 3 h. P. gingivalis suspended in OPTI-MEM was added to the Cell Cycle inhibitor Ca9-22 cells at an MOI of 1:100

and further incubated at 37°C in 5% CO2 for 1 h. Unattached bacteria were removed by washing with PBS three times. OPTI-MEM containing 200 μg/ml of metronidazole and 300 μg/ml of gentamicin was added to the plates and they were incubated for 1 h. The cells were washed twice with PBS, and then 1 ml of sterile distilled water per well was added and the cells were suspended persistently by pipetting to disrupt them. The lysates were serially diluted and plated on 5% horse blood agar plates (Poa Media, Eiken Chemical) and then incubated anaerobically at 37°C for 10 days. Colony-forming units (CFU) of invasive P. gingivalis in cells were then enumerated. Silencing of Rab5 gene RG-7388 purchase Ca9-22

cells were transfected with 100 pmol siRNA specific for Rab5 (RAB5A-HSS108978, Invitrogen) or control siRNA (Stealth™ RNAi Negative Control Medium GC Duplex, Invitrogen) using Lipofectamine 2000 reagent, as described by the manufacturer (Invitrogen). Then, selleck chemical expression of Rab5 in the cells was examined by Western blotting using a monoclonal antibody to Rab5. Next, Rab5 siRNA-transfected Ca9-22 cells were incubated with P. gingivalis ATCC 33277 (MOI =100) for 1 h. Viable P. gingivalis in the cells was determined as described above. Immunostaining Treated Ca9-22 cells were fixed with 4% formaldehyde for 10 min. Nonspecific binding of antibodies was

blocked by incubation with 5% sheep serum in 10 mM Tris pH 7.6, 150 mM NaCl, and 0.05% Tween20 (TBS-T) for 1 h, and then the cells were incubated overnight at 4°C with a primary antibody (antiserum for P. gingivalis whole cells, mouse monoclonal antibody specific for ICAM-1) in TBS-T. After washing with buffer A (10 mM Tris pH 7.6, 300 mM NaCl, and 0.5% Tween20) 6 times, the cells were treated with a secondary antibody (anti-rabbit IgG-Alexa 555 or anti-mouse IgG-Alexa 555 and anti-rabbit IgG-Alexa 633) in buffer A for 1 h. Cells were then observed by DNA ligase a confocal laser scanning microscope (Leica microsystems, Welzlar, Germany). Some Ca9-22 cells were transfected with vectors containing genes of GFP alone (control), GFP-Rab5 (S34N) (inactive form of Rab5), and GFP-Rab5 (Q79L) (active form of Rab5). To clarify whether P. gingivalis cells are in the epithelial cells, a z-series with 0.5 μm-intervals was scanned and images of the x-z and y-z planes were reconstructed with the orthogonal section tool. Western blotting TNF-α-treated and non-treated Ca9-22 cells and THP-1 cells were lysed in SDS-PAGE sample buffer, separated by SDS-PAGE, and transferred onto Immobilon-P Transfer Membranes (Millipore, Billerica, MA). The membranes were blocked with PVDF Blocking Reagent for Can Get Signal (Toyobo) in TBS-T for 1 h at room temperature and then incubated with antibodies to TNFRI, TNFRII, Rab5 and ICAM-1 overnight at 4°C.

Biochim Biophys Acta 504:142–152PubMedCrossRef Ivanov AG, Sane PV

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