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The inducible nitric oxide synthase (iNOS) is associated with inflammatory processes and cancer formation through production of nitric oxide (NO). However, the clinical importance of the expression of iNOS in oral cancer remains unclear. In the present study, we examined whether up-regulation of the iNOS gene can affect growth and metastasis of an oral cancer cell line (B88t cell) in vitro and in vivo.', 'We constructed an expression vector containing sense-oriented murine iNOS cDNA with pcDNA3.1. We transfected B88t cells with the sense expression vector to up-regulate the expression of the iNOS gene in the sense transfectants.', 'The expression of iNOS protein was up-regulated in the sense transfectants and that up-regulation of the iNOS gene exerted a growth inhibitory effect on B88t cells in vitro and in vivo. Moreover, up-regulation of the iNOS gene markedly inhibited the migration of cancer cells in a Boyden chamber. Furthermore, up-regulation of the iNOS gene dramatically inhibited metastases to the cervical lymph node in vivo.
Does overexpression of iNOS gene suppress the tumorigenicity and metastasis of oral cancer cells?

Energy needs in infants are decreased after surgery because of growth inhibition (resulting from catabolic stress metabolism), decreased insensible losses, and inactivity. Using standardized formulas that account for growth, activity, and insensible losses during this stress period can lead to overfeeding in excess of 200% of the actual measured requirement. Overfeeding during this acute injury period can result in increased CO2 production from lipogenesis. This study determined the effects of a reduced rate of mixed caloric repletion on infant energy use during the early postoperative period.', 'C-reactive protein (CRP), oxygen consumption (VO2), carbon dioxide production (VCO2), measured energy expenditure (MEE), and total urinary nitrogen (TUN) were measured serially in seven infants (average age, 78 days) during the first 72 hours after abdominal or thoracic surgery. Nonprotein respiratory quotient (RQnp), and values for oxidation of carbohydrate (Ce) and fat (Fe) were calculated. Injury severity was stratified based on serum CRP concentrations of > or = 6.0 mg/dL (high stress) or < 6.0 mg/dL (low stress). Recovery from acute stress was analyzed by comparing studies in which CRP had decreased to < or = 2.0 mg/dL (resolving stress group) with those in which CRP values were greater than 2.0 mg/dL (acute stress group).', 'Average total caloric intake (64.56 +/- 18.51 kcal/kg/d; approximately 50% of predicted energy requirement) exceeded average MEE (42.90 +/- 9.98 kcal/kg/d) by approximately 50%. Average TUN was 0.18 +/- 0.07 g/kg/d (high stress 0.2 +/- 0.05 versus low stress 0.16 +/- 0.09 g/kg/d). Average RQnp was 1.05 +/- 0.13 and average Ce was 37.28 +/- 16.86 kcal/kg/d. The average calculated Fe was 0.0 +/- 12.27 kcal/kg/d, reflecting approximately equal amounts of fat oxidized compared with fat generated from excess glucose (lipogenesis). When individual studies were analyzed at a CRP cutpoint of 2.0 mg/dL, overfeeding (RQ > 1.0) was significantly less likely in the resolving (2/6 studies, 33.4%) versus acute stress (9/13 studies, 69.2%, Z test P < .001) group. Five of seven (5/7) patients (9/19 individual studies) had negative Fe values (average -9.89 +/- 10.02) reflecting net lipogenesis. The RQnp for these nine studies was 1.14 +/- 0.11 versus 0.97 +/- 0.09 for the remaining 10, and this difference was significant (P < .01). A significant correlation existed between carbohydrate intake and VCO2 (Pearson r = .6951, P < .01). In addition, there was a good correlation between carbohydrate intake and VCO2 (Pearson r = .6591, P < .01). The coefficient of variation for MEE was 8.0% (low stress) versus 30.2% (high stress).
Do early postoperative alterations in infant energy use increase the risk of overfeeding?

Direct interaction between Red blood cells (RBCs) and platelets is known for a long time. The bleeding time is prolonged in anemic patients independent of their platelet count and could be corrected by transfusion of RBCs, which indicates that RBCs play an important role in hemostasis and platelet activation. However, in the last few years, opposing mechanisms of platelet inhibition by RBCs derived nitric oxide (NO) were proposed. The aim of our study was to identify whether RBCs could produce NO and activate soluble guanylate cyclase (sGC) in platelets.', "To test whether RBCs could activate sGC under different conditions (whole blood, under hypoxia, or even loaded with NO), we used our well-established and highly sensitive models of NO-dependent sGC activation in platelets and activation of purified sGC. The activation of sGC was monitored by detecting the phosphorylation of Vasodilator Stimulated Phosphoprotein (VASP(S239)) by flow cytometry and Western blot. ANOVA followed by Bonferroni's test and Student's t-test were used as appropriate.", 'We show that in the whole blood, RBCs prevent NO-mediated inhibition of ADP and TRAP6-induced platelet activation. Likewise, coincubation of RBCs with platelets results in strong inhibition of NO-induced sGC activation. Under hypoxic conditions, incubation of RBCs with NO donor leads to Hb-NO formation which inhibits sGC activation in platelets. Similarly, RBCs inhibit activation of purified sGC, even under conditions optimal for RBC-mediated generation of NO from nitrite.

Do erythrocytes activate purified and platelet soluble guanylate cyclases even in conditions favourable for NO synthesis?