An extremely well-preserved dinosaur (Cf. Edmontosaurus sp.) found in the Hell Creek Formation (Upper Cretaceous, North Dakota) retains soft-tissue replacement structures and associated organic compounds. Mineral cements precipitated in the skin apparently follow original cell boundaries, partially preserving epidermis microstructure. Infrared and electron microprobe images of ossified tendon clearly show preserved mineral zonation, with silica and trapped carbon dioxide forming thin linings on Haversian canals within apatite. Furthermore, Fourier transform infrared spectroscopy (FTIR) of materials recovered from the skin and terminal ungual phalanx suggests the presence of compounds containing amide groups. Amino acid composition analyses of the mineralized skin envelope clearly differ from the surrounding matrix; however, intact proteins could not be obtained using protein mass spectrometry. The presence of endogenously derived organics from the skin was further demonstrated by pyrolysis gas chromatography mass spectrometry (Py-GCMS), indicating survival and presence of macromolecules that were in part aliphatic (see the electronic supplementary material).
[1] Volcanoes discharge a range of inorganic major gas species (e.g., H 2 O, CO 2 , SO 2 , and CO) not only during eruptions but also during quiescent phases through fumarolic and diffuse degassing in their craters and on their flanks. The emission of organic trace gases from volcanoes is similarly not expected to be restricted to discrete fumarolic gas discharges alone. To test this hypothesis, we have sampled soil gas emissions for organic compounds and determined CO 2 fluxes along a profile extending from the vegetated base of the active La Fossa cone (Vulcano Island, Italy) over the unvegetated volcanic flank and up into the crater rim and base and then continuing over fumarolic areas. The results indicate that the majority of volatile organic compounds in the soil gas show significant increases in concentration toward the crater and fumaroles and that diffuse emissions contribute significantly to the volcanic halocarbon source strength. Emissions of the halocarbon CFC-11 (CCl 3 F) correlate well with soil CO 2 fluxes measured on site (R 2 = 0.89, slope = 1.42 ± 0.1) and both increase toward the crater and fumaroles. Other ozone-depleting substances were found in concentrations significantly above those found in field and system blanks, including CH 3 Br, CH 3 Cl, CH 3 I, C 2 H 5 Br, and chlorinated benzenes. Abundances ranged from upper pptv to ppmv; for example, the maximum observed CFC-11 concentrations were 1200 pptv in diffuse emissions and 3700 pptv in dry fumarolic gas (average dry air is 268 pptv). On the basis of these results the natural volcanic source strength of halocarbon emissions to the atmosphere requires reevaluation, and in some cases, correction to higher values. Global average fumarolic and diffuse halocarbon source strengths were estimated and scaled to known global volcanic fumarolic and diffuse CO 2 flux data. Among these were CFC-11 (8.56 ± 4.7 Â 10 À6 Tg y À1 ), CH 3 Br (0.98 ± 0.47 Â 10 À6 Tg y À1 ), CHCl 3 (94.9 ± 27.6 Â 10 À6 Tg y À1 ), and CCl 4 (3.41 ± 1.0 Â 10 À6 Tg y À1 ).
Impaired pulmonary release of nitric oxide (NO) is one of the characteristic phenotypic changes of vascular cells in pulmonary hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with primary pulmonary hypertension. NOS-dependent whole body NO production was assessed by giving an intravenous infusion of L-[15N]2-arginine (50 µmol/min for 30 min) and measuring isotopic urinary enrichment of 15N-nitrite and 15N-nitrate. Four female patients with no signs of infection were recruited and compared with 6 age-matched control subjects. Mean 12-hour excretion of 15N-nitrite and 15N-nitrate in the total urine over 36 h was smaller in patients than in control subjects (57.2 ± 27.6 vs. 229.1 ± 65.2 nmol/mmol creatinine, p< 0.01, Mann-Whitney U test, respectively). Neither mean 12-hour excretion of 14N-nitrite and 14N-nitrate (51.6 ± 10.0 vs. 72.4 ± 10.0 µmol/mmol creatinine, p = 0.3) nor glomerular filtration rates (84.5 ± 15.8 vs. 129.7 ± 16.0 ml/min, p = 0.1) were different between patients and control subjects. Our results suggest that either basal NOS-dependent whole body NO production is impaired or excess NO metabolism occurs in patients with primary pulmonary hypertension.
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