Then, cell cultures were pretreated for 24 hours before XRT with 1 μM simvastatin alone, C225

alone (10 nM C225 for FaDu cells or 30 nM for A431 cells), or with the two drugs. Next, cell cultures were either irradiated (2 Gy) or subjected to mock irradiation in the presence or absence of the drugs. Colonies were stained with crystal violet. Clonogenic cell survival was calculated as the ratio between the number Selumetinib of colonies presented after irradiation and the number of cells plated, which was then normalized by the clonogenic efficiency of the untreated controls. Note that when XRT was applied, clonogenic cell survival was the survival after 2 Gy, which is the most useful clinical marker of intrinsic radiosensitivity. To generate tumor xenografts, 106 cells suspended in 100 μl of medium were injected into subcutaneous tissues on the right hind limb of 6- to 8-week-old female athymic Swiss nu/nu mice (Harlan, Gannat, Selleckchem Ruxolitinib France). Cells were injected on a Monday and left to grow for 7 days, moment when the treatments began. Tumor growth was measured—π/6 × (large diameter) × (small diameter)2—twice weekly. Mice were killed when the tumor volume reached 1200 mm3, when the mice showed moderate to severe toxicities, or when significant differences between groups were observed. All experimental procedures were approved by the Institutional Animal

Care and Ethics Committee. The mice received fractionated XRT, C225, and simvastatin. XRT was selectively delivered from Monday to Friday for 2 weeks using the 6-MV X-ray beams at doses of 20 to 30 Gy depending on type of experiment, in 10 fractions, 1 fraction each day. On the first day of treatment, C225 was intraperitoneally injected 6 hours before

irradiation at doses of 1 mg per animal to allow the antibody to have time to saturate the EGFR. Next, C225 was administered on days 3, 7, and 10 at doses of 0.5 mg per animal 2 hours (together with simvastatin or its vehicle) before irradiation as a maintenance C225 dose. Simvastatin (50 mg/kg) was administered orally on a daily basis for 12 days 2 hours before irradiation. Mice were randomly allocated to receive XRT plus C225 or XRT, C225, and simvastatin as well as to receive single treatments with XRT, C225, or simvastatin alone. In addition, a group N-acetylglucosamine-1-phosphate transferase of mice treated in parallel was killed on day 4 to obtain tumor samples for immunofluorescence. Semi-confluent cell cultures were pretreated for 48 hours with C225 and simvastatin in FBS-free medium and then irradiated with a single dose of 5 Gy. Twenty minutes after irradiation, cell cultures were rinsed in ice-cold phosphate-buffered saline (PBS) and lysed in radioimmunoprecipitation assay buffer with protease and phosphatase inhibitors. Vehicle and mock irradiation were provided as controls. Protein concentration in the lysates was determined by the Pierce BCA Protein Assay Kit (Thermo Scientific, Rockford, IL).

, 1998). In Gulf killifish and sea trout, our findings were check details the same: the response to oil exposure was a decreased number of circulating lymphocytes, which makes fish more susceptible to infectious diseases. Laboratory studies of the effects of petroleum products on fish immune responses were conducted before the Deepwater Horizon disaster and findings include increased or decreased macrophage respiratory burst, depending on the chemical, the amount used and the fish species (reviewed in (Reynaud and Deschaux, 2006)). Expression analysis of immune related genes following petroleum exposure showed that they were up-regulated (Bowen et al., 2007). Genomic analysis

of Gulf killifish liver tissue demonstrated that the oil exposure caused significant biological changes (Whitehead et al., 2011). RNA-Sequence analysis of Gulf killifish from another oil-exposed site indicated that the circulating (peripheral) leukocytes were undergoing immune stress (Garcia et al., 2012). Historically,

sampling surveys demonstrated that fish from polluted waters had a higher incidence of lesions. More specifically, hydrocarbon exposure results in decreased mucus production and increased epidermal lesions and parasitism as well as impaired function of many immune responses (reviewed in Austin, 1999). Alligator gar are large, euryhaline fish that can be found throughout Gulf coastal and in-land waters. They were selected as a target species because they are bi-modal breathers Ribociclib chemical structure and could be exposed to emulsified anti-PD-1 antibody or surface contaminants. Gar are also a top-predator and may demonstrate accumulated effects of oil in the ecosystem. However, they may not demonstrate the effects seen in the other estuarine fish because they cover expansive areas and move in and out of contaminated waters. This is probably why peripheral blood smears from alligator gar in Terrebonne Bay appeared normal. Conversely, Gulf killifish live in marshes, and usually stay in a localized area (McClane, 1978). They occupy a niche that is very vulnerable to contamination, and would remain there during the

spill. It is likely this is why peripheral blood leukocyte changes were observed in these fish. After the Gulf oil spill, surface water analyses conducted by the US Environmental Protection Agency (EPA) and the Mississippi Department of Environmental Quality (MDEQ) determined that daily air and water quality was within normal ranges at monitoring sites along the MS Gulf Coast (Beasley et al., 2012). During the spill, the majority of oil was emulsified and entered the deep waters of the Gulf (Camilli et al., 2010). A large sub-surface plume was followed for months. This plume contained an amount of petroleum hydrocarbon that was double the amount of naturally occurring seepage (Camilli et al., 2010). Damaged and killed coral beds in the path of the predicted deep-water oil plume demonstrated these systems were specifically impacted by Macondo oil (White et al.

This may rely on an understanding of what is good, hence including societal views as well as ecological views (see Mee et al., 2008). Furthermore, Odum (1985) described stress in the system as a set of EIGHTEEN adverse characteristics and so a healthy system by definition should be the converse of those characteristics (see Elliott and Quintino, 2007). The management of an ecosystem and an understanding of the way in which it changes under human influences requires a large amount of data, information and knowledge about the structure and functioning of the system; this can

be described as NINE stages which then allows management decisions to be made (Box 4; McLusky and Elliott, 2004). Such a framework, which is sufficiently generic to cover all human

activities, will encourage managers to obtain Proteasomal inhibitors the appropriate information for management. By accumulating information in progressing from Stage 1 to Stage 9, conservation and environmental protection bodies can then determine the effects of human activities on the marine system. Each of the ‘decisions’ relates to the way in which the ecosystem functions and selleck chemical the behaviour of materials or activities placed in the environment. For example, the placing of dredged material into the sea after dredging will have an effect which depends on the nature of the receiving environment (i.e. whether PFKL it has water currents above a threshold speed), and on the nature of the material being dumped (e.g. whether it is sand or mud). However, The Ecosystem Approach is necessary to ensure that all aspects are taken into account and thus that the overall health of systems and the ecosystem services that they deliver are recognised and protected. To detect change then requires monitoring the system – when to assess and what to assess – although we have further complicated this to result in TEN types of monitoring: • Surveillance monitoring – a ‘look-see’ approach which begins without deciding what are the end-points followed by a post hoc detection (a posteriori) of trends and suggested management action. As emphasised here, the aim of

marine management is to protect the whole system although, again as shown here, this is complex achievement. Given this complexity, we often deconstruct the ecosystem into a set of component parts, assess each of them in relation to any stressors and then aim to recombine our assessments to give the management of the whole system – this is what we previously called a ‘deconstructing structural approach’ as used for the European Water Framework Directive (Borja et al., 2010b). The WFD, adopted in 2000, concentrated on assessing deviation from Good Ecological Status by FIVE Biological Quality Elements (phytoplankton, macroalgae, macrophytes, benthic fauna and fishes) plus the chemical and physical characteristics.

T.L.B., R.F.L., E.I.M., and M.-B.M. planned experiments and analyses, T.L.B., R.F.L., and I.U.K. collected data, T.L.B. and R.F.L. analyzed data, and T.L.B.,

E.I.M., and M.-B.M. wrote the paper, with input from the other authors. We thank V. Frolov and R. Skjerpeng for programming; M.P. Witter for advice on histology; and A.M. Amundsgård, K. Haugen, E. Henriksen, Alpelisib concentration K. Jenssen, E. Kråkvik, B.B. Løfaldli, and H. Waade for technical assistance. This work was supported by the Kavli Foundation, a student research grant from the Faculty of Medicine at the Norwegian University of Science and Technology, an Advanced Investigator Grant from the European Research Council (“ENSEMBLE,” grant agreement 268598), and Centre of Excellence and FRIPRO grants from the Research Council of Norway. “
“Green woodhoopoes (Phoeniculus purpureus) live in groups consisting of a dominant breeding pair and up to six nonbreeding helpers of both sexes [ 10]. Each group defends a year-round territory (mean ± SE area = 23.5 ± 1.7 hectares) in thickly forested valleys

[ 11], and they generally forage and move around this territory as a single unit [ 12]. Group members roost communally in tree cavities every night, which yields vital thermoregulatory benefits [ 13], and use one of the same cavities for nesting [ 10]. Each territory contains only a small number (mean ± SE = 6.9 ± 2.9) of suitable tree cavities [ 10], and these represent the limiting resource for woodhoopoe survival PDGFR inhibitor and reproduction: groups will move rapidly into previously unoccupied areas of forest if nest boxes are provided [ 14]. Interactions between groups are common and involve all group members contributing to alternating choruses (or “rallies”) [1], which on rare occasions escalate to physical fighting [15]. Around 97% of intergroup interactions (IGIs) between neighbors take place within

100 m of shared territory boundaries, termed zones of conflict [16]. We found that cavities in zones of conflict were used for roosting significantly more often than would be expected by chance (Wilcoxon signed-ranks test: Z = 2.05, n = 12, p = 0.041; Ribonucleotide reductase Figure 1A). Groups with a greater involvement in IGIs, compared to those that interacted less with their neighbors, used zone-of-conflict roosts relatively more often than predicted from their availability (Spearman rank correlation, IGI rate: rs = 0.59, n = 12, p = 0.042; proportion of time engaged in IGIs: rs = 0.62, n = 12, p = 0.032; Figure 1B). Woodhoopoe IGIs are highly variable in duration (1–45 min) and exhibit a bimodal distribution: “short” IGIs (>57% of cases), usually on territory boundaries, are decided within 5 min and primarily involve information exchange about current group structure and potential breeding opportunities, while “extended” IGIs (∼30% of cases), which develop when there is a conflict over territory space, take >15 min to resolve and usually involve a territorial intrusion [15].

Traditionally, only mast cell CPA and plasma CPU have been considered as regulatory enzymes within the M14 family of metallocarboxypeptidases [33]. More recently it was proposed that CPA6, an extracellular matrix protease secreted in some areas of human and mouse brains, plays a role in the regulation

of neuropeptides [17]; also, we have shown that the major kininase of the rat MAB perfusate is identical with rat CPB1 [23], another prototypical pancreatic metallopeptidase. Vorinostat Thus, our present demonstration that rat MAB CPA1 and CPA2 are capable of processing Ang peptides extends the current evidence of the participation of metallocarboxypeptidases in regulatory pathways. The peculiar proteolytic profiles displayed by CPA1 and CPA2 toward Ang peptides probably reflect the proposed evolutionary events that have allowed these enzymes to diverge from one another with respect to substrate specificity, resulting in overlapping and complementary preferences [10]. Thus, Ang I was efficiently acted upon Selleckchem NVP-BGJ398 by CPA1, forming Ang-(1-7) by a three-step pathway with Ang-(1-9) and Ang II as intermediates (Fig. 5A); confirmatory evidence of this sequential mode of action of CPA1 has been provided by the formation of the end-product Ang-(1-7) in analogous reactions when either Ang-(1-9) or Ang II, the intermediates

in the conversion of Ang I to Ang-(1-7), were used as substrate for the enzyme (Fig. 5B and C). On the other hand, only Ang-(1-9) was released upon incubation of Ang I with CPA2 (Fig. 6A); in agreement with this result, the substrates Ang II and Ang-(1-9) were negligibly hydrolyzed by CPA2 under the conditions described in Fig. 6B and C. Comparison of the catalytic efficiencies of the CPA1- and CPA2-mediated conversions of Ang II to Ang-(1-7) indicates a value approximately 200-fold higher for the former enzyme (Fig. 7), consistent with the results of Ang II cleavage by these enzymes shown in Fig. 5 and Fig.

6B; such a discrepancy between kinetic parameters of CPA1 and CPA2 toward Ang II is significantly larger than those observed for synthetic substrates having carboxyl-terminal Phe residue [10], the same terminal residue CYTH4 of Ang II. It should also be noted here that the Km value for the CPA1-catalyzed conversion of Ang II to Ang-(1-7), as determined in Fig. 7, is of the same order of magnitude as that of the analogous reaction catalyzed by ACE2 [28], a carboxypeptidase for which there is compelling evidence of participation in the RAS [34]; thus, the binding affinity of rat CPA1 for Ang II seems compatible with the participation of this enzyme in the formation of Ang-(1-7) under physiological conditions. However, the contribution of CPA1 to the in vivo generation of Ang-(1-7) in the rat mesenteric vascular bed is likely to depend on factors beyond that of the enzyme affinity for Ang II, among which the actual CPA1 activity and the presence of circulating carboxypeptidase inhibitors.

The ABS-OOTF agreed (Level 2 Consensus) that intravitreal anti-VEGF therapy is useful to suppress radiation-induced neovascular glaucoma, radiation maculopathy, and optic neuropathy. Therapy is used to suppress transudation, thus ameliorate edema and counter neovascularization [119], [120], [121], [122] and [123]. However, although these techniques are widely used, the ABS-OOTF selleck chemicals llc recognizes that no published prospective randomized or large-scale studies examined the effects relative to initial radiation dose, dose rate, or source. The literature also contains two alternative approaches to the treatment of radiation

retinopathy. Laser photocoagulation in the form of posterior tumor demarcation resulted in sector devascularization best seen on fluorescein angiography. This technique along with sector pan retinal photocoagulation has been reported to slow or prevent radiation retinopathy by two independent centers [124] and [125]. Treatment converted slow ischemia within and anterior to the target to scar. In theory, laser devitalization of the ischemic tumor and treated retina may decrease

intraocular production of VEGF. However, brachytherapy also affects the eyelids, eyelashes, conjunctiva, tear production, corneal surface integrity, sclera, and ocular muscles [8], [100], [126] and [127]. Within the eye, radiation can cause iritis, uveitis, synechiae, Depsipeptide datasheet neovascular glaucoma, cataract, posterior neovascularization, hemorrhage, retinal detachment, retinopathy, and optic neuropathy. The most common late sight

limiting posterior segment complication is radiation maculopathy. Unusual complications include persistent strabismus and scleral thinning. All the aforementioned side effects can result in loss of vision and quality of life. The ABS-OOTF recognize that there exists no comprehensive staging system for the ophthalmic side effects of radiation therapy. Although many of these findings are fundamentally, albeit less specifically, classified by the United States National Cancer Institute (Cancer Therapy Evaluation Program, Common Terminology Criteria for Adverse Events, Version 4.0, DCTD, National Cancer Institute, National MycoClean Mycoplasma Removal Kit Institute of Health, Department of Health and Human Services (http://ctep.cancer.gov)), the ABS-OOTF recommends that a radiation-specific ophthalmic side effect staging system should be developed to improve communication for patient care, research, and publication. This presentation of ABS-OOTF guidelines for ophthalmic plaque brachytherapy offers both consensus and controversy. We recommend that brachytherapy should be performed by a team composed of a skilled subspecialty-trained plaque surgeon, radiation oncologists, and medical physicists in experienced subspecialty centers.

Similar positive LD signals were observed for the Zn(bpy)2 and Cd(bpy)2 complexes at the time of mixing (Fig. S3). Therefore, the possibility of ligand intercalation between the DNA base-pairs can be rejected. With

time, the magnitude of the LD spectrum decreased gradually and the signal was almost diminished 20 min after mixing, suggesting that dsDNA became so flexible and shortened that it could not be oriented in the flow. Fig. 5 shows the decrease in LD intensity at 260 nm as a function of time. Although the LD intensity at 260 nm of the dsDNA-Cu(bpy)2 Sunitinib mw adduct decreased gradually with time, reaching a zero magnitude within 20 min, that of the dsDNA-Zn(bpy)2 and dsDNA-Cd(Bpy)2 adduct remained almost constant (curves b and c), indicating that the flexibility and length of DNA are unaffected by the presence of either Zn(bpy)2 or Cd(bpy)2. This suggests that, in addition to the cleavage of scDNA probed by electrophoresis, the latter two metal complexes were unable to cleave the DNA. The decrease in LD intensity at 260 nm in the presence of the Cu(bpy)2 complex cannot be explained by simple first or second order kinetics as it was evaluated by the residuals. The residual from single component exponential decay is shown in the lower panel as an example. The sum of the two first order kinetics which corresponds to the sum of two exponential curves, LD(t)=a1exp(−t/τ1)+a2exp(−t/τ2)LDt=a1exp−t/τ1+a2exp−t/τ2were

this website the best to elucidate the decay of the LD signal. The decay curve analysis for the dsDNA-Cu(bpy)2 adduct is shown in Fig. 5. The goodness of fit was evaluated by the residuals. As observed from the residuals (Fig. 5, low panel), the decay curve of the dsDNA-Cu(bpy)2 adduct consisted of two exponential

components, i.e., τ1 = 1.42 and τ2 = 7.16 min, the mean of the three measurements, with their relative amplitude of a1 = 0.324 and a2 = 0.676, respectively. The relevant reaction times τ1 and τ2 correspond to the rate constant of the first order reactions k1 = 0.71 min− 1 and k2 = 0.14 min− 1, respectively. As observed for scDNA, various ROS may affect the efficiency of the cleavage of dsDNA. Fig. 6 shows the effect of ROS scavengers on the decreasing profile of the LD signal of the dsDNA-Cu(bpy)2 adduct. At a glance, it is clear that the presence of tiron drastically suppresses the Vasopressin Receptor cleavage (curve e, Fig. 6). The catalase also had a large inhibition effect (curve d, Fig. 6). The two component curve fitting resulted in τ1 = 1.22 and τ2 = 16.66 min with their relative amplitude of a1 = 0.298 and a2 = 0.702, respectively. The two reaction time correspond to the two first order reaction constants, k1 = 0.82 min− 1 and k2 = 0.060 min− 1, respectively. Sodium azide had an intermediate inhibitory effect on dsDNA cleavage. The reaction times, τ1 = 1.45 (a1 = 0.231) and τ2 = 10.59 min (a2 = 0.769), were obtained from that fit. The inhibitory effect of DMSO was the weakest.

Brachytherapy cases were randomly selected for review and data abstraction using lists of eligible patients provided by the treating facilities. Eligibility criteria for

inclusion in the survey were as follows: (1) biopsy-proven adenocarcinoma of the prostate, (2) treatment that consisted of a permanent interstitial implantation, (3) treatment received Sirolimus mw during 1 year (2007), and (4) treatment in which the use of androgen-deprivation therapy in conjunction with radiotherapy was acceptable. Patients who had a prior radical prostatectomy or were treated for recurrent/metastatic disease were excluded. The characteristics of these patients as well as brachytherapy treatment details are summarized

in Tables 1 and 2. Trained research associates performed onsite reviews PD98059 cell line of the medical records of selected cases. Information about patient characteristics; tumor characteristics; staging workup; and brachytherapy treatment details, including isotope, seed strength, number of seeds, and PD, were collected and recorded in an online database. Digital Imaging and Communications in Medicine CT images, contours of the prostate and rectum, and radiation dose files (which were extracted from a variety of treatment planning systems) were remotely deidentified and submitted from the sites to a control center at the Image-Guided Therapy QA center (ITC) located in St. Louis, MO. The deidentified CT images were then uploaded from the ITC to a treatment planning system (Variseed Varian Brachytherapy, Charlottesville, VA) at the reference expert institution

for this study (Memorial Sloan–Kettering Cancer Center) where the prostate and rectal anatomy were recontoured by one physician (LM) and checked carefully for accuracy by another (MJZ). Because these CT scans were obtained 2–6 weeks after the ADP ribosylation factor implantation procedure, a urinary catheter was not in place and delineation of the urethra for contouring purposes was not obtained. Based on the new contours and the seed locations, dose–volume histograms were generated and dosimetric evaluation was performed for each of these cases. Dosimetric parameters analyzed included %V100 prostate (percent volume of the prostate that received the PD), D90 prostate (dose delivered to 90% of the prostate expressed in percent of the PD), %V150 prostate (percent volume of the prostate that received 150% of the PD), V100 rectum (percent volume of the rectum that received the PD), and D2cc rectum (dose to 2 cc of the rectum expressed in percent of the PD).

65 Mammalian models like the mouse and rat are considered extremely valuable models of disease that typically mimic human conditions.

Their anatomy and cell biology are well conserved and techniques such as genetic fate mapping can facilitate the tracking of cell types during regeneration. Furthermore, these models are essential to evaluate efficacy and toxicity of pharmaceuticals for AKI treatment, and remain the gold standard in preclinical trials. Rodent AKI models include IRI as well as exposure to chemical agents such as gentamicin and, thus, can be used to model the outcomes of different insults.66 However, scientists are still faced with several limitations when studying AKI in these mammalian

kidneys. Access to the rodent kidney requires surgery. For the Buparlisib in vivo most part, this eliminates real-time visual monitoring of the renal tissues in living animals, with the only current exception being a very small population of renal tubules and vessels near the surface of the organ.67 For a number of reasons, the zebrafish has emerged as a relevant vertebrate that can be used to address several voids in the AKI field. Research in zebrafish embryos and adults has shown that the pronephros and mesonephros kidney forms, respectively, are valid models for gentamicin-based AKI studies.68, 69, 70, 71, 72 and 73 Zebrafish nephrons in embryos and adult animals show a conserved

make-up with mammals (detailed further in following sections).10 and 74 Zebrafish larvae are optically transparent, allowing microscopic observation Smad3 signaling along the entire length of the kidney. Additionally, zebrafish serve as a suitable experimental model in that they breed frequently, produce large numbers of progeny, and the embryos develop ex utero. 75 They also progress very rapidly through embryogenesis and organogenesis. C1GALT1 For example, the embryonic kidney has formed 1 day after fertilization and the pronephric tubules begin filtration of the blood by the second day of life. 76 One important aspect of AKI research resides in the possibility of identifying small molecules with therapeutic potential to aid in repair and regeneration. The zebrafish has become an appealing tool for such small molecule screens.75, 77 and 78 Because the embryo is small in size, relatively small quantities of compounds are needed for testing, and embryos can be kept alive for days without added nutrients because they utilize maternal food deposits. The adult zebrafish can be injected with small amounts of compounds to interrogate regeneration because of the small adult mass,79 enabling findings from the embryo to be tested in an adult organ setting. Comparable screening of pharmaceutical molecules in rodents would require an extraordinary amount of time, chemical compounds, as well as residential space.

3A) and induced a 2.7-fold decrease in IL-6 protein HDAC inhibitor levels (p < 0.001) ( Fig. 3B). In contrast, after 1 h, 10 nM cortisol (simulating physiological stress levels) promoted increase IL-6 mRNA expression (129% compared to control) ( Fig. 3A) and protein levels ( Fig. 3B) in SCC9 cells, but these changes did not reach significance. These cortisol effects were blocked by glucocorticoid inhibitor Mefipristone (data not shown). SCC25 cells

did not exhibit a significant response to cortisol treatment. Specifically, SCC25 cells treated with 1000 nM cortisol at 6 h produced 292.2 ± 17.40 pg/mL of IL-6, resulting in a 1.25-fold decrease compared to the control (p < 0.05) ( Fig. 3D). In these same cells, lower IL-6 mRNA levels were detected at 1 h with 100 nM cortisol (131.1 ± 0.03% compared to the control) and 1000 nM cortisol (152.1 ± 2.7%), while an increase in IL-6 mRNA levels took place at 24 h using 10 nM cortisol (138 ± 12.96%) and 100 nM cortisol (147 ± 28.75%), but these results were not significant ( Fig. 3C). Similar results were found in SCC15 cells, in which lower cortisol concentrations (1 and 10 nM) did not determine large variations in IL-6 mRNA levels, whereas high concentrations simulating pharmacological selleckchem concentrations (e.g., 1000 nM) decreased IL-6 expression (but these results were not significant) (Fig. 3E). To examine

the effects of stress hormones on OSCC cell proliferation, SCC9 and SCC15 cells were treated with different doses of NE and cortisol, and cell proliferation was assayed by MTT at 6, 24, and 48 h. The SCC25 cell line was not assayed by MTT because it did not respond well (absence of cell growth) to culture in serum-reduced medium (0.1% FBS). Stimulation of SCC9 and SCC15 cells with physiological NE stress levels (10 μM) induced an enhancement of 170 ± 17.7% (p < 0.05) and 124 ± 13.7% (p < 0.05) in cell proliferation at 6 h compared with non-treated cells, respectively ( Fig. 4A). These

NE-induced effects of SCC9 and SCC15 cells were not significant at subsequent times (24 and 48 h) (data not shown). In SCC9 cells, treatment with pharmacological levels of cortisol (1000 nM) produced at later time point (48 h) a rise of approximately 200 ± 36.1% in cell proliferation (p < 0.05) ( Fig. 4B). Cortisol doses that simulate stress conditions (10 nM) induced at 48 h an increase Dimethyl sulfoxide in cell proliferation in SCC9 (non-significant) ( Fig. 4B) and in SCC15 cells (135 ± 17.5%; p < 0.05) ( Fig. 4B). There was no significant increase in the cell proliferation index after 6 and 24 h of stimulus with cortisol (data not shown). Real-time PCR assays confirmed that SCC9, SCC15, and SCC25 cells express mRNA for β1- and β2-AR (Fig. 5A). To determine whether the increase in IL-6 expression was mediated through β-adrenergic receptors, the cell lines were pre-treated with a nonspecific β antagonist (propranolol), at the time point of maximum mRNA IL-6 expression (10 μM NE at 1 h).