Infrared Emission from Photodissociation of Methyl Formate [HC(O)OCH3] at 248 and 193 nm: Absence of Roaming Signature.

Following photodissociation at 248 nm of gaseous methyl formate (HC(O)OCH3, 0.73 Torr) and Ar (0.14 Torr), temporally resolved vibration-rotational emission spectra of highly internally excited CO (ν ≤ 11, J ≤ 27) in the 1850-2250 cm-1 region were recorded with a step-scan Fourier-transform spectrometer. The vibration-rotational distribution of CO is almost Boltzmann, with a nascent average rotational energy (ER0) of 3 ± 1 kJ mol-1 and a vibrational energy (EV0) of 76 ± 9 kJ mol-1. With 3 Torr of Ar added to the system, the average vibrational energy was decreased to EV0 = 61 ± 7 kJ mol-1. We observed no distinct evidence of a bimodal rotational distribution for ν = 1 and 2, as reported previously [Lombardi et al., J. Phys. Chem. A 2016, 129, 5155], as evidence of a roaming mechanism. The vibrational distribution with a temperature of ∼13000 ± 1000 K, however, agrees satisfactorily with trajectory calculations of these authors, who took into account conical intersections from the S1 state. Highly internally excited CH3OH that is expected to be produced from a roaming mechanism was unobserved. Following photodissociation at 193 nm of gaseous HC(O)OCH3 (0.42 Torr) and Ar (0.09 Torr), vibration-rotational emission spectra of CO (ν ≤ 4, J ≤ 38) and CO2 (with two components of varied internal distributions) were observed, indicating that new channels are open. Quantum-chemical calculations, computed at varied levels of theory, on the ground electronic potential-energy schemes provide a possible explanation for some of our observations. At 193 nm, the CO2 was produced from secondary dissociation of the products HC(O)O and CH3OCO, and CO was produced primarily from secondary dissociation of the product HCO produced on the S1 surface or the decomposition to CH3OH + CO on the S0 surface.

Elevated serum matrix metalloproteinase-3 and -7 in H. pylori-related gastric cancer can be biomarkers correlating with a poor survival.

BACKGROUND: Helicobacter pylori (H. pylori) infection up-regulates the expression of matrix metalloproteinases (MMPs), which may be involved in chronic inflammation, ulceration, and even cancer development. This study aimed to test if serum levels of MMP-3, -7, and -9 are correlated with different clinical outcomes in H. pylori-infected subjects and if these are predictive of progression to H. pylori-related gastric cancer. METHOD: Two hundred one patients, 28 with H. pylori-negative gastritis and 173 with different H. pylori-positive gastrointestinal diseases (46 gastritis, 43 duodenal ulcers, 29 gastric ulcers, and 55 gastric cancers) were assessed for serum MMP-3, -7, and -9 titers by enzyme-linked immunosorbent assay and validated to their correlations with the different clinical features and survival of patients with H. pylori-positive gastric cancer. RESULTS: Among the H. pylori-infected subjects, gastric cancer patients had higher serum levels of MMP-3 and MMP-7 than those with duodenal ulcer and gastritis (P < 0.05). For gastric cancer patients, concomitant elevated MMP-3 (>14 ng/ml) and MMP-7 (>4.5 ng/ml) independently correlated with lymph node invasion (P < 0.05) and could be predictive to have shorter 2- or 5-year survivals (log rank test, P = 0.006). CONCLUSION: Concomitant elevations of MMP-3 and MMP-7 serum levels in the H. pylori-infected gastric cancer patients could serve as potential biomarkers to correlate with poor survival.

Decoy receptor 3 ameliorates experimental autoimmune encephalomyelitis by directly counteracting local inflammation and downregulating Th17 cells.

To investigate the therapeutic potential of decoy receptor 3 (DcR3) in multiple sclerosis (MS), we used intrathecal (IT) administration of DcR3 into C57/BL6 mice with experimental autoimmune encephalomyelitis (EAE). DcR3 significantly ameliorated EAE symptoms as shown by a lower clinical score and less inflammation in the spinal cord. The expression of TNF-alpha, IFN-gamma, and IL-17 was lower in the spinal cord in IT DcR3-treated mice. Flow cytometry showed a drastic reduction in IL-17-producing CD4 T cells, slightly fewer IFN-gamma producing CD4 T cells and more IL-4-producing CD4 T cells isolated from the central nervous system (CNS) of IT DcR3-treated mice than of controls. Myelin oligodendrocyte glycoprotein (MOG)-specific T cell proliferation was significantly inhibited in DcR3-treated mice. The IL-17 concentration was lower and the IL-4 concentration higher in the supernatants of MOG-stimulated splenocytes from DcR3-treated mice. An adoptive transfer study showed that splenocytes from DcR3-treated mice retained this disease-inhibiting ability. Our data suggest that DcR3 has potential as a suppressor of CNS inflammation in EAE, which may be attributed to either direct inhibition of CNS inflammation or suppression of encephalitogenic Th17 cells. In conclusion, we demonstrate a therapeutic effect of DcR3 in EAE, suggesting its potential for treating human MS.

Overexpression of c-erb-B2 proteins in tumor and non-tumor parts of gastric adenocarcinoma--emphasis on its relation to H. pylori infection and clinicohistological characteristics.

BACKGROUND/AIMS: This study was designed to test whether c-erb-B2 overexpression can be related to H. pylori infection or clinicohistological characteristics of patients with gastric cancers. METHODOLOGY: One hundred patients with gastric cancer were included. Their gastric specimens were evaluated for the presence of H. pylori infection and overexpression of c-erb-B2 on both tumor and non-tumor mucosa. The clinicohistological characteristics, including stage, histological subtype, cell differentiation, and locations of gastric cancer were reviewed. RESULTS: Seventy-five patients (75%) had H. pylori infection. The H. pylori infection rate was higher in the patients with non-cardiac cancers than those with cardiac cancers (87.5% vs. 25%, P < 0.05), higher in the patients with intestinal-type cancers than those with diffuse-type cancers (78.8% vs. 53.3%, P < 0.05). The overexpression of c-erb-B2 on gastric cancers was not significantly different between patients with and without H. pylori infection (30.7% vs. 36%, P = NS). Overexpression of c-erb-B2 on the gastric cancer tissues increased as the tumor stage turned upward (stage I: 10%; II: 23.3%, III: 32.5%, IV: 55%, P < 0.05), and highest in the poorly differentiated cancers (56.6%). Only patients with advanced stages as II to IV had c-erb-B2 overexpression on the non-tumor part of stomach (P < 0.05). CONCLUSIONS: H. pylori infection is closely related with the non-cardiac, intestinal-type gastric cancers, but not with the c-erb-B2 overexpression on the gastric cancer. As c-erb-B2 overexpression on gastric cancer is significantly related with poor tumor differentiation and advanced stage, and it thus implicates a poor prognosis and late event of carcinogenesis.

Stool antigen assay to screen H. pylori infection and to assess the success of 3-Day and 7-Day eradication therapy in the patients with partial gastrectomy.

BACKGROUND: Even after partial gastrectomy, Helicobacter pylori may persist in the residual stomach but be less abundant in the bacterial load. H. pylori stool antigen is a reliable noninvasive tool to detect H. pylori infection in patients without gastrectomy. We thus test whether [1] the course of H. pylori eradication therapy could be diminished [2]; stool antigen can effectively detect H. pylori infection for the patients with gastrectomy. METHODS: One hundred and eight patients who had undergone partial gastrectomy were enrolled to receive panendoscopy and provided stool samples for H. pylori stool antigen within 3 days after endoscopy. The H. pylori-infected patients were then randomized to receive either a 3- or 7-day triple therapy for H. pylori eradication. Six weeks later, to evaluate the success of H. pylori eradication, patients received a follow-up endoscopy and again provided stool samples for H. pylori stool antigen. RESULTS: Seventy out of 108 patients, proven to have H. pylori infection, were evenly randomized into 3-day and 7-day therapy groups. The H. pylori eradication rates were similar between the 3-day and 7-day triple therapy (90.9 vs. 93.8%, p >.05). Before therapy, the H. pylori stool antigen was 93% sensitive and 100% specific to detect H. pylori. After therapy, H. pylori stool antigen remain 100% sensitive and 88.3% specific to detect the failure of eradication therapy. CONCLUSION: H. pylori stool antigen is a highly reliable tool to screen H. pylori infection before therapy and to assess the success of eradication therapy in partial gastrectomy patients. To eradicate H. pylori infection for patients with partial gastrectomy, the duration of triple therapy can be shortened.