These results support the participation of hydroxyl radicals in a

These results support the participation of hydroxyl radicals in arsenic-induced

disturbances in the central nervous system. In this connection, an interesting route to produce H2O2 was explained by the oxidation of As(III) to As(V) which, under physiological conditions, results in the formation of H2O2 (a source of damaging hydroxyl radical): equation(20) H3AsO3 + H2O + O2 → H3AsO4 + H2O2  (ΔrGΘ = −40.82 kcal/mol) The above reaction is spontaneous and exergonic with an estimated standard reaction free energy change for H2O2 formation of −40.82 kcal/mol (−170.87 J/mol). In addition to ROS, arsenic exposure can also initiate the generation of RNS. Several conflicting reports concerning arsenic-induced production of NO have been published Y-27632 in vitro (Shi et al., 2004). One report concluded that there was no cadmium-induced

increase in NO generation in hepatocytes and human liver cells, which inhibited inducible NO synthase gene expression in cytokine-stimulated human liver cells and hepatocytes (Germolec et al., 1996). In another report, arsenite was found to inhibit inducible NO synthase gene expression in rat pulmonary artery smooth muscle cells (Kodavanti et al., 1996). Similarly, a third study with low levels of arsenite reported no change in intracellular concentration of Ca(II) as well as no NO generation as detected by EPR spectroscopy (Barchowsky et al., 1999). GSH is a very effective cellular antioxidant and plays an important learn more role in maintaining cellular redox status. In addition, GSH level is a good marker of oxidative stress of an organism (Halliwell and Gutteridge, 2007). Several papers have reported decreased levels of GSH

after exposure to arsenic. It was reported that following oral intake of arsenic, Astemizole the GSH concentration was significantly decreased in the liver of male Wistar rats (Maiti and Chatterjee, 2001). After 6 months exposure to arsenic, hepatic GSH and the enzymes glucose-6-phosphate dehydrogenase and GPx were significantly lowered in mice. Overall, from these studies follow that GSH possibly acts as an electron donor for the reduction of pentavalent to trivalent arsenicals and that arsenite has high affinity to GSH. The exact molecular mechanism of arsenic toxicity and carcinogenesis is still not known. Current views of molecular mechanisms of arsenic toxicity involve genetic changes, the involvement of increased oxidative stress, enhanced cell proliferation and altered gene expression. Arsenic is known to induce hypoxia signalling pathways. For example in prostate cancer cells treated with arsenite induced HIF-1alpha expression in a concentration- and time-dependent manner, whereas the level of HIF-1beta remained unaffected (Posey et al., 2008). The VEGF protein level was also elevated. ROS formation was linked with the activation of the PI3K/Akt pathway and the subsequent induction of HIF-1alpha and VEGF.

Collaboration recently established with SPRFMO allowed the recove

Collaboration recently established with SPRFMO allowed the recovery of almost 900,000 t that had not been reported to FAO over the 2003–2009 period, including 650,000 t of jack mackerel caught by vessels flagged by Vanuatu [40]. Although in the Article

XI of the FAO Constitution is clearly stated that all member countries should communicate regularly statistics and other technical information available to the government to allow FAO compiling and disseminating data on global trends, not all countries submit their annual fishery statistics to FAO. Failing to report is mainly due to the selleck compound fact that for several countries is difficult to collect reliable catch statistics in a continuous manner, as it is a costly activity that needs skilled personnel and in many

cases production points (i.e. landing sites) cover a large geographical area and are dispersed. However, there are also cases in which data have been collected but trivial problems in communication (e.g. turnover of the responsible Selleck AZD2281 officer, etc.) hamper the transmission of information to FAO. FAO has been recording modalities of submission and evaluating the catch data received for the last ten statistical inquiries (2000–2009 data). The introduction of electronic questionnaires since the 1999 inquiry certainly contributed to the improvement of more timely reporting as the average number of submissions within the deadline increased from 51 in 2000–2003 to 72 in 2007–2009 (Fig. 3). Despite FAO’s efforts, unfortunately the number of non-reporting countries has remained stable, although countries PIK3C2G or territories that never

submitted catch data during the decade are not many but more than half of the countries did not report at least once. The quality of fishery data is known to be very uneven among countries. Besides data on timing of submission, also information on species breakdown and an evaluation of data consistency have been recorded since the 2000 inquiry. Rank values from 4 to 1 were assigned to all countries for the three indicators, which were then combined in a ‘General evaluation’ index of country’s submission for each year. The ‘General evaluation’ score obtained by each country for 2009 has been plotted in a matrix against the ‘Per capita supply’ of fishery products [2], which was considered as a valid indicator of the importance of fisheries in each country as unfortunately data on fishery contribution to national GDP are not consistently available for all countries. Data submitted or non-reported were considered inadequate in relation to the relative importance of capture fishery for over half of the countries.

Em conclusão, os critérios de diagnóstico de HAI, à semelhança do

Em conclusão, os critérios de diagnóstico de HAI, à semelhança do que acontece com outras patologias semelhantes, destinam-se a suprir a falta de um verdadeiro gold standard diagnóstico. No nosso trabalho, demonstrámos que, na prática clínica, perante uma suspeita de HAI, Seliciclib clinical trial os CDS podem ser uma opção inicial, mas deverão usar-se também os critérios clássicos, sobretudo se com os CDS se obtiver uma pontuação inferior a 6. No entanto, são necessários mais estudos, se possível multicêntricos, de modo a abranger um maior número de doentes, para avaliar definitivamente a possibilidade de substituição dos critérios clássicos pelos simplificados. Proteção de pessoas e animais. Os autores declaram que para esta investigação

não se realizaram experiências em seres humanos e/ou animais. Confidencialidade dos dados. Os autores declaram ter seguido os protocolos de seu

centro de trabalho acerca da publicação dos dados de pacientes e que todos os pacientes incluídos no estudo receberam informações suficientes e deram o seu consentimento informado por escrito para participar nesse estudo. Direito à privacidade e consentimento escrito. Os autores declaram que não aparecem dados de pacientes neste artigo. Os autores declaram não haver conflito de interesses. “
“O espectro da doença hepática alcoólica (DHA) é bastante variável, mesmo dentro do seu continuum evolutivo que engloba a esteatose, a esteato-hepatite e a cirrose hepática. A esteato-hepatite alcoólica é um paradigma desse facto, pois cursa, desde formas ligeiras e apenas diagnosticáveis histologicamente, Ipilimumab mw até um quadro clínico grave, com prognóstico sombrio por falência hepática aguda, que se designa por hepatite alcoólica aguda (HAA)1. A sua patogenia envolve a agressão hepática efetuada pelo álcool, através da sua metabolização em acetaldeído, formação de radicais livres de oxigénio, peroxidação lipídica e formação de adutos com proteínas e ácido desoxiribonucleico, associada a alteração da permeabilidade intestinal com passagem de endotoxinas para a circulação portal. Estes processos condicionam uma ativação das células de Kupffer e libertação

buy Tenofovir de citocinas (TNF-α, IL-1, prostaglandinas, leucotrienos), aumento de expressão de moléculas de adesão e quimiocinas, levando ao recrutamento de leucócitos polimorfonucleares, com o desencadear de uma resposta imune local, cuja intensidade e autoperpetuação caracteriza a HAA1. A apresentação clínica desta entidade é muito variável. Talvez devido a esta variabilidade, a HAA tende a ser subvalorizada e subdiagnosticada pelos clínicos, apesar de estar associada a uma mortalidade significativa2. Apesar de vários relatos prévios de icterícia após episódios de consumo excessivo de álcool, o termo «HAA» só foi usado pela primeira vez por Beckett em 19613. Mais recentemente, o termo «aguda» passou a ser desencorajado, pois, na maior parte dos casos, representa uma exacerbação da doença crónica subjacente – a DHA4.

In fact, as I was examining the abdomen of the last such patient

In fact, as I was examining the abdomen of the last such patient I saw with these complaints, he looked up at me and said, “you know, Dr. Brandt, you are the first doctor who has touched me.” In addition to being embarrassed for our profession, I thought, as the kids of today say, “Oh, my God.” That patient’s comments prompted me to write this page on how to touch an abdomen. Of course, touch is preceded by inspection and after the patient has unclothed, inspection is performed for scars (trauma, surgery—either

laparotomy or laparoscopy), XL184 chemical structure hyper- or hypopigmentation (radiation, melanoma, Addison’s disease, Kohlmeir-Degos disease), and asymmetry (hernias, organomegaly, masses). After touch, the examiner arrives upon the subject of this page: Gentle Stroking and Delicate Pinching. Most examiners, when pressing on the abdomen and eliciting pain, assume the tenderness arises within the abdominal cavity and fail to consider that it may be from an injured muscle, an irritated or entrapped nerve, hernia, rectus sheath hematoma, or even inflamed fat. Cyriax, in 1919, was the first to note this important observation that anterior abdominal wall pain may arise from structures other than

the underlying viscera. To distinguish intra- from extra-abdominal conditions, I suggest, after inspection, the following routine: (1) Begin with a very gentle stroking of the abdominal skin, using as light a touch as possible, passing rapidly from inferior to superior (left, middle, and right vertical striping) and selleck then left to right (upper, middle, and lower horizontal striping), including all 9 anatomic Isotretinoin regions of the abdomen (right and left hypochondriac, lumbar, and iliac, and epigastric, umbilical, and hypogastric). Hyperalgesia or dysesthesia can thus be elicited and reveals any area with abnormal sensation or innervation. This technique alone can pick up the

early stages of shingles, a nerve entrapment syndrome or neuropathy, or can even identify an intraabdominal pathologic condition with peritoneal irritation. (2) I then follow this gentle stroking with a deeper stroke as if I were creating a propagated wave form with my finger. This enables me to determine the texture of the skin and muscle; is it smooth, granular, lumpy, freely mobile, intact? I then proceed to gently pinch my fingers together, thereby grabbing a small pannus of fat; I gently squeeze it, again in each of the 9 anatomic regions of the abdomen; how else can one diagnose painful fat syndrome? (3) Now I will probe more deeply, again mindful of the anatomic regions. The edges of the liver and possibly the spleen are found along the way and noted for their palpable characteristics such as firmness, smoothness, and nodularity.

15 Consequently, the ongoing phase III efficacy trial with this s

15 Consequently, the ongoing phase III efficacy trial with this strain is conducted with higher dose (105 ffu) and a 3-dose schedule (6, 10 and 14 weeks).15 It can be argued that one study in South Africa and Malawi with monovalent rotavirus vaccine (RV1, marketed as Rotarix) did not detect significant differences in vaccine immunogenicity or efficacy on pooled analysis between the cohort receiving two vaccine doses and the cohort receiving three doses.3 However, there was a slight but

non-significant trend toward higher seroconversion rates and vaccine efficacy with the three-dose schedule, and these differences were more marked in South Africa (81.5 (55.1–93.7) vs 72.2 (40.4–88.3)) than in Malawi (49.7 (11.3–72.2) this website vs 49.2 (11.1–71.7)).3 The two-dose schedule used in this trial was 10 and 14 weeks instead of 6 and 10 weeks.3 Administering rotavirus vaccines at younger ages could further lower the immunogenicity of the vaccines, because of the potential for greater interference of maternal antibody and enhanced replication of the oral poliovirus vaccine.3 In the above African

study with RV1, the researchers accepted that the study was not powered to detect differences in dose schedule.3 Furthermore, there have been low seroconversion rates (58.3%; 95% CI: 48.7; 67.4) with two doses of RV1 in comparison Amisulpride with three-dose schedule of RV5 (82.4% (CI; 75; 90%)) and 116E (89.7% (42.4; 80.6%)) in immunogenicity studies in India.15, 16 and 17 In the click here RV1 trial, the first dose was administered between 8 and 10 weeks (mean age – 8.7 weeks)

and the second dose between 12 and 16 weeks (mean age – 13.4 weeks).16 Hence, there is no immunogenicity data for 6 and 10 weeks administration or data on interference with simultaneous OPV administration from India. It is important when examining immunogenicity data to point out that although seroconversion is not a direct proxy for efficacy, it does demonstrate that the virus is able to colonize the infant gut and induce a robust immune response. Figure options Download full-size image Download as PowerPoint slide According to the WHO Ad-hoc Group of Experts on rotavirus vaccines,18 most countries with high rotavirus disease incidence or high under-5 mortality rates (where children would particularly benefit from robust protection from rotavirus infection) have 6, 10, 14 week EPI schedules. If rotavirus vaccines are to be co-administered with OPV in a setting with an EPI vaccination schedule beginning at 6 weeks of age, the second dose of RV1 may not be sufficient to provide adequate immunity against severe rotavirus disease.


may then bind reactivated content to current


may then bind reactivated content to current experience, resulting in an integrated trace. Following integration in hippocampus, memory models may be updated with new content as needed through direct hippocampal inputs PD0325901 to mPFC [18]. Through this process, mPFC may come to represent integrated memories that have been abstracted away from individual episodes (i.e., schema) over time 18 and 25. A number of studies suggest that memory integration persists into post-encoding rest [26] and sleep [27], with offline consolidation processes facilitating generalization across episodes. Specifically, hippocampus-driven reactivation during slow-wave sleep is thought to transform memories, allowing connections to be formed among representations co-activated in neocortex [28]. This

process is thought to promote both the integration of new information into existing memories and abstraction across episodes in neocortical regions, particularly mPFC [28]. Memory integration has largely positive effects on behavior (though see Box 2 for examples of negative behavioral consequences). Below, we review recent work highlighting these benefits across a number Antidiabetic Compound Library order of cognitive domains. While the effects of integration on behavior are largely beneficial, a few studies have uncovered negative consequences of integration. For example, integration may lead to false memories (i.e., through overgeneralization) [59•], and memory misattributions 5, 22•, 55 and 56. Interestingly, patients with ventral mPFC lesions show reduced false memories relative to healthy control participants for words that were never seen but are thematically related to a studied word list

[59•], consistent with the notion that ventral mPFC constructs generalized memory representations. Integration may also explain the phenomenon of memory misattribution, in which an episodic experience is incorrectly attributed to a different encoding DOK2 context than the one in which it occurred (e.g., as measured by intrusions; Box 1). Misattributions may occur when prior knowledge is reactivated and updated with the current experience to the detriment of memory accuracy. One fMRI study [5] used neural decoding to quantify the neural reinstatement of the context associated with prior memories (List 1) during new learning (List 2). Results showed that greater evidence for reactivation of the List 1 context was associated with more misattributions of List 2 words to List 1. Another study [22•] showed that when participants reactivated a prior experience during new encoding, ventral mPFC and hippocampal engagement was associated with later memory misattributions, consistent with a role for these regions in linking experiences across time. Perhaps the most familiar and widely studied form of memory integration stems from Tolman’s seminal work on cognitive maps [7].

01 M, pH 6 01) at 70 °C for 10 min, followed by incubation in 0 0

01 M, pH 6.01) at 70 °C for 10 min, followed by incubation in 0.075 g/ml trypsin (Difco Laboratories, Detroit, USA) in PBS at 37 °C for 5 min. Then, the sections were pre-incubated with 10% normal donkey serum (NDS) (Chemicon, Temecula, USA) in PBS-G. All antibodies and the Vectastain ABC Standard alkaline phosphatase mix (ABC-AP) (Vector Laboratories, Burlingame, CA, USA) were diluted in 2% NDS. To detect GFP, the sections were incubated overnight at 4 °C with a polyclonal rabbit-anti-GFP antibody (1:300) (Invitrogen/Molecular Probes, Eugene, OR, USA). Subsequently, biotinylated

find more donkey-anti-rabbit (1:500) (Jackson Labs, West Grove, PA, USA) was added. Next, the sections were treated with ABC-AP, and washed with Tris–HCl (pH 8.2). Fast Blue substrate (Sigma Chemical CO, St Louis, MO, USA) was freshly prepared, and applied to the sections. The reaction was stopped in demineralized water (Milli-Q pore system, Millipore SA, Molsheim, France), and the sections were washed in PBS and pre-incubated again for double-staining with the following primary mouse monoclonal antibodies: (A) Anti αSMA (Sigma Chemical CO), 1:1600, 1 h at room temperature to detect myofibroblasts. Next goat-anti-mouse-AlexaFluor-594

learn more (1:200, 1 h at room temperature) (Invitrogen/Molecular) was added. Finally, the sections were washed, and the nuclei were stained with DAPI (Roche Diagnostics Nederland BV, Almere, The Netherlands). A 1,4-diazabicyclo[2.2.2]octane solution (DABCO, Sigma Chemical CO) solution in Tris–buffered glycerin was used as anti-fading agent. Slides were stored in the dark at 4 °C. Photographs were taken on a Carl Zeiss Imager Z.1 system (Carl Zeiss Microimaging Gmbh, Jena, Germany). GFP photos were acquired under bright field conditions. The other sections were photographed with fluorescent settings. The GFP images were inverted and merged with the fluorescent images to reveal co-localization using ImageJ (National Institutes of Health, Bethesda, Maryland, Hydroxychloroquine concentration USA). The fraction of GFP-positive mononuclear cells was determined in the blood of GFP-transgenic rats and recipient rats by flow cytometry. In three sections of each mucoperiosteal tissue sample, αSMA-positive cells

and nuclei were counted in the wound and control area within a frame with a width of 50 μm and a depth of 300 μm. GFP-positive and GFP/αSMA double-positive cells were counted in a larger area of 200 μm wide because they are less abundant. The epithelium was excluded. The fraction of the other bone marrow-derived cell types in the mucoperiosteum was estimated in three rats with a high fraction of GFP-positive cells in the wound tissues. Three tissue sections were used to determine the number of double-positive cells as described above. In the tissue sections from the skin similar countings were performed but the selected areas had a depth of 500 μm and a width of 300–600 μm. Epithelial cells, cells in blood vessels, muscle cells, and hair follicle cells were excluded.

Specifically, we asked for ratings of 15 recreational activities

Specifically, we asked for ratings of 15 recreational activities according to 1) their perceived commonness and harmfulness to the coastal environment, and 2) their perceived influence on visitors’ wellbeing in terms of mood and excitement. Perceived changes in marine awareness after a visit were also included. The sample consisted of 122 participants: 25 coastal experts (7 men, 18 women) and 97 coastal users (24 males,

72 females, 1 not stated). The majority (40%) of the coastal experts fell into the 25–30 age category, whilst the majority (30%) of the coastal users fell into the 51–60 age category. Coastal experts were professionals predominantly employed by conservation Selleckchem Roscovitine charities such as the National Trust. Their roles linked directly to the management of coastlines and/or involved engaging with the public in these coastal environments, specifically rocky shores, for instance arranging events such as rock pool rambles. This specialised sample was recruited using the snowball sampling technique. They were recruited via professional networking (e.g. at conferences) and were sent an email with the study information and survey link to an online questionnaire that they were asked to forward

onto others within the same profession. Of those who were directly contacted by the researcher, 34% responded. This resulted in a sample of coastal Sulfite dehydrogenase experts who, on average, had spent eight years working in the coastal field (SD = 6.57; range = 1–26 years). Their coastal sites varied from the Isles of Scilly to Teesside in the UK, with the majority based in Devon (44%). For this study, coastal users were defined as individuals that often visit the coast but do not have expertise or work in a profession that involves working on the coast. A convenience

sample was recruited using a staff announcement that was placed on Plymouth University’s (an institution located near rocky shores in the Southwest of England) internal website that all employees see when accessing any online services. The advert included a short description about the study, the inclusion criteria (that participants often visit the coast and are not coastal experts) and the link to the survey. Even though this sample is not representative of the national population, it did comply with the coastal user definition above; with the majority visiting once or twice a month (38%) or once every couple of months (26%), with no coastal based occupations reported.

After 3 h the blood was collected from the tail of the animals an

After 3 h the blood was collected from the tail of the animals and the activity of creatine kinase (CK) in plasma was determined using a commercial kit (Sigma) protocol. The activity was expressed as U/L at 30 °C, considering 1 Unit as 1 μmol of NADH/min. To confirm the LmLAAO myotoxic effect, this assay was done with samples from two different samples of LmLAAO (Test 1 and Test 2), obtained by purification protocol 2. After collection of blood from the tail of CD-1 mice injected in the femoral quadriceps to determine the myotoxic activity, animals were sacrificed. The muscles injected with either PBS or LmLAAO were dissected and samples were routinely processed

for histological observation, as described above. The cytotoxic activity of LmLAAO was tested on the breast adenocarcinoma line (MCF-7), and on

a gastric adenocarcinoma line (AGS). The cells were maintained in Dulbecco’s essential medium supplemented with 10% fetal bovine serum, 2 mmol/L glutamine, 100 IU/mL penicillin and amphotericin B at 37 °C in a humidified atmosphere containing 7% CO2. For the experiments, cells were cultured in 96-well plate (15,000 cells/well) and left overnight. LmLAAO at different concentrations (75, 37.5, 18.8, 9.4, 4.7, 2.3 and 1.2 μg/mL) was added to adhered cells and incubated for 24 h. Assays were performed in the presence of catalase (0.1 mg/mL). The assessment buy BIBW2992 of LmLAAO for toxic activity on the cells was performed using the technique of MTT colorimetric reduction clonidine (Mosmann, 1983). The tests were performed in triplicate and expressed as percentage of cell lysis. The half inhibitory concentration (IC50), mean and standard deviation were calculated using the software Graphpad Prism 5.0. Promastigote forms (L. braziliensis) were cultivated in medium 199 supplemented with 10% fetal bovine serum, penicillin and streptomycin and maintained at 22 °C. Parasites in the stationary phase were deposited in 96-well microplates at a concentration of 1 × 106 parasites/mL and

incubated with different concentrations of LmLAAO (0.5, 2, 8 and 32 μg/mL). Controls were performed with water, medium 199, catalase (0.1 mg/mL) and the parasites strain. After 24 h, the parasite viability was determined using the technique of MTT colorimetric oxidation as described by Muelas-Serrano et al. (2000). The tests were performed in triplicate for each concentration of LmLAAO and controls. Results were expressed as percentage of cell lysis (%CL) and the IC50, mean and standard deviation were calculated by Graphpad Prism 5.0 software. Trypomastigotes forms of B5 clone of CL Brener strain were grown in culture of LLCMK2 cells and the assays were performed according to the methodology described by Vega et al. (2005), in which the parasites were incubated in 96-well microplate in the presence of different concentrations of LmLAAO (0.5, 2, 8, 32 μg/mL), at 4 °C, for 24 h.

As observed in the case of cytokines expression regulation, this

As observed in the case of cytokines expression regulation, this result may suggest that the cortisol effect on the cell cycle proteins may be dependent on the hormone levels. Further studies are necessary to evaluate Trichostatin A nmr which underlying mechanisms are activated in OSCC cells after variations of the systemic and tissue levels of cortisol in response to chronic and acute stress conditions. In addition to confirming that OSCC cell lines express β1- and β2-AR, we have also demonstrated that these receptors are expressed in specimens of OSCC, oral leukoplakia, and normal oral mucosa. The β-adrenergic receptors are

members of the large family of G protein-coupled receptors (GPCR), and their activation involves protein-tyrosine-kinase-activated pathways, as well as cyclic-adenosine-monophosphate (cAMC)-linked pathways. It has been shown that several types of cancer express β-AR, which may affect proliferation and migration as well as induce metastasis (Askari et al., 2005, Cakir et al., 2002 and Shin et al., 2007). β1-AR expression in OSCC BMS-354825 mw and oral leukoplakia specimens has not yet been reported. Quantitatively, the mean β1-AR expression level in OSCC was approximately 3- and 2-fold those encountered in the normal mucosa and leukoplakia, respectively. These findings suggest that the changes in epithelial and mesenchymal cells

during oral carcinogenesis can be accompanied by modifications in β1-AR expression. Moreover, β1-adrenergic receptor agonists, such as NE, could determine more pronounced effects in neoplastic tissues compared to normal tissues. β2-AR expression in OSCC biopsies

has been previously analyzed by Shang et al. (2009). Immunohistochemistry analysis showed that 67.7% of OSCC cases were positive for β2-AR protein expression, while only 20% of adjacent normal mucosa specimens were positive for β2-AR staining CYTH4 (Shang et al., 2009). However, β1-AR expression was not evaluated. In our cases, only one specimen of normal mucosa was negative for β2-AR, and there was no expressive difference in its expression when tumor and normal mucosa specimens were compared. This distinct result in terms of β2-AR expression obtained by us and Shang et al. may be due to the use of different methods. In real-time PCR assay other cells of the tumor microenvironment that also express β-ARs in addition to epithelial cells are also included in the analysis. Previous studies have shown that patients with oral cancer can have high psychological distress levels (Kugaya et al., 2000 and Chen et al., 2009). The effects of stress-related hormones on oral cancer cells are still poorly understood. Although this study has limitations because it is composed mainly of in-vitro assays, the results reveal that stress-related mediators, mainly NE at concentration compatible with physiological stress levels in humans, can upregulate IL-6 expression and induce OSCC cell proliferation.