Differences between the surface chemical properties of hydrogen-and nitrogen-treated samples of an activated carbon were quantified using several complementary techniques. Calorimetric studies conducted at 303 K revealed that the sample treated in N2 at 1223 K adsorbs a great deal of oxygen with unusually high differential heats. In fact, both the quantity and the heat of adsorption increased when the treatment temperature was raised from 773 to 1223 K. In contrast, samples treated in H2 adsorbed less and less O2 as the temperature of treatment was raised; after treatment at 1223 K, virtually no O2 adsorption occurred. At the same time the H/C ratio in the H2-treated samples decreased with increasing treatment temperature. Point of zero charge measurements revealed that only H2 treatments at high temperature (>1073 K) create basic (hydrophobic) surfaces which are stable after prolonged air exposure. These findings are consistent with the notion that the removal of oxygen in the form of CO and CO2 during high-temperature N2 treatment leaves unsaturated carbon atoms at crystallite edges; these sites are very active for subsequent oxygen adsorption. In contrast, high-temperature H2 treatment accomplishes three tasks: (a) it also removes surface oxygen; (b) it stabilizes some of the (re)active sites by forming stable C-H bonds; (c) it gasifies the most reactive unsaturated carbon atoms. The relative contributions of these three effects depend on the temperature of H 2 treatment. The carbon surface resulting from high-temperature H2 treatment is stable against subsequent O2 adsorption in ambient conditions.

High Slug expression is closely correlated with poor prognosis in patients with BLBC. We speculate that this may be attributed to the involvement of Slug in the EMT of BLBC.

Further insight into important aspects of the chemical surface properties of activated carbons is provided by rationalizing the differences in O2 adsorption and desorption behavior of hydrogen-and nitrogentreated activated carbons. The effects of heat treatment on the electrochemical behavior of these carbons were also instrumental in elucidating the nature and the distribution of carbon active sites. Activated carbon surfaces stabilized with hydrogen at 950 °C adsorb very little O 2 at room temperature but the graphene layers are terminated with many free carbon active sites because significant O2 adsorption does take place at 150 °C. Furthermore, the low-coverage differential heats of adsorption on sites accessible at 150 °C were lower than those on sites accessible at 25 °C. The role of these free carbon sites in determining the basicity of activated carbons was also addressed. On the basis of the important finding that the point of zero charge exhibits a maximum at intermediate heat-treatment temperatures, it is proposed thatsin addition to the delocalized basal-plane π electronssthe localized π electrons at graphene edges (e.g., inplane divalent sigma pairs) act as Lewis bases that interact with protons in aqueous solution.

Background:Tumour necrosis factor-α-induced protein 8 (TNFAIP8) has been recently documented in various malignancies, but its role in epithelial ovarian cancer (EOC) remains unknown.Methods:Tumour necrosis factor-α-induced protein 8 expression was determined by real-time reverse transcription PCR and western blot analysis. Tumour tissues, consisting of serous, mucinous, endometrioid and clear cell histotypes, from 202 EOC patients (International Federation of Gynecologists and Obstetricians I–IV) who underwent primary cytoreduction were collected. Then, we examined the immunohistochemical expression of TNFAIP8 and evaluated its clinical significances.Results:Tumour necrosis factor-α-induced protein 8 overexpression was significantly associated with high histologic grade (P=0.005), large residual tumour size (P=0.014), recurrence (P=0.024) and response to chemotherapy (P<0.001). Multivariate analysis showed that TNFAIP8 overexpression was independently correlated with the presence of lymph node (odds ratio (OR): 4.129; 95% confidence interval (CI): 1.491–11.435; P=0.006) and intraperitoneal metastasis (OR: 2.209; 95% CI: 1.174–4.156; P=0.014). Moreover, results revealed that the status of TNFAIP8 expression was an independently prognostic factor for both cancer-specific survival (hazard ratio (HR): 1.852; 95% CI: 1.322–2.594; P<0.001) and disease-free survival (HR: 1.724; 95% CI: 1.235–2.407; P=0.001) in patients with EOC.Conclusion:The present data provide evidence that TNFAIP8 predicts EOC metastasis and poor survival, highlighting its potential function as a therapeutic target for EOCs.

Toll-like receptors (TLRs) have crucial roles in innate immunity, functioning as pattern-recognition receptors. TLR13 recognizes a conserved sequence from bacterial 23S rRNA and then triggers an immune response. Here we report the crystal structure of the mouse TLR13 ectodomain bound by a 13-nt single-stranded (ss) RNA derived from 23S rRNA. The ssRNA induces TLR13 dimerization but assumes a stem-loop-like structure that is completely different from that in the bacterial ribosome but nevertheless is crucial for TLR13 recognition. Most of the RNA nucleotides are splayed out to make base-specific contacts with the concave surface of TLR13, and RNA-specific interactions are important to allow TLR13 to distinguish RNA from DNA. Interestingly, a viral-derived 16-nt ssRNA predicted to form a similar stem-loop-like structure also induces TLR13 activation. Together, our results reveal the structural mechanism of TLR13's sequence- and conformation-specific recognition of ssRNA.