Academic literature on the topic 'Ringyō keiei'

Jerome, E. Heidi, Keiji Enzan, Dominique Douguet, Dachuan Lei, Gary Jesmok, Carol W. Johnson, Maritza Neuburger, and Norman C. Staub. Chronic interleukin-2 treatment in awake sheep causes minimal or no injury to the lung microvascular barrier. J. Appl. Physiol. 81(4): 1730–1738, 1996.—Interleukin-2 (IL-2) is reputed to cause a “vascular leak syndrome.” We studied pulmonary hemodynamics and lymph dynamics in six sheep treated for 7 days with IL-2 (1.8 million IU/kg twice daily or 1.8 million IU/kg each day as a continuous infusion). Lung lymph flow increased from 4.8 ± 2 ml/15 min pre-IL-2 to 14.4 ± 6.8 ml/15 min on the seventh day of IL-2. The lymph-to-plasma protein concentration ratio was unchanged (0.70 ± 0.06 vs. 0.63 ± 0.13). The plasma-to-lymph equilibration half-time of radiolabeled albumin was 2.0 ± 0.6 h pre-IL-2 and 1.0 ± 0.7 h on day 7 of IL-2. Pulmonary arterial pressure was 24 ± 7 cmH2O pre-IL-2, increased to 32 ± 4 cmH2O on the fourth day of IL-2, and returned to 29 ± 5 cmH2O on the seventh day of IL-2. Extravascular lung water was normal (4.07 ± 0.25 g/g dry lung). To clearly determine whether the increase in lung lymph flow was due to hemodynamic changes or to increased leakiness of the microvascular barrier, we volume loaded six sheep with lactated Ringer solution before and after 3 days of IL-2 treatment (1.8 million IU/kg twice daily). Lung lymph flows increased fivefold during 4 h of crystalloid infusion compared with baseline and were higher after 3 days of IL-2. However, lymph-to-plasma protein concentration ratios decreased to the same low levels pre- and post-IL-2 (0.39 ± 0.06 vs. 0.41 ± 0.10), indicating an intact microvascular barrier. Extravascular lung water was elevated (5.56 ± 0.39 g/g dry lung) but was not different from lung water in three volume-loaded control sheep (4.87 ± 0.53 g/g dry lung). We conclude that IL-2 causes minimal or no injury to the pulmonary microvascular barrier and that volume expansion during IL-2 treatment can cause hydrostatic pulmonary edema.

Keiji Maruoka of Kyoto University found (Organic Lett. 2010, 12, 1668) that the diazo amide 1 derived from the Oppolzer sultam condensed with the imine 2 to give the aziridine 3 with high stereocontrol. Andrei K. Yudin of the University of Toronto observed (Angew. Chem. Int. Ed. 2010, 49, 1607) that the unprotected aziridine aldehyde 4, which exists as a mixture of dimers, condensed smoothly with the Ohira reagent 5 to give the alkynyl aziridine 6. David M. Hodgson of the University of Oxford successfully (Angew. Chem. Int. Ed. 2010, 49, 2900) deprotonated the azetidine thioamide 7 to give, after allylation, the azetidine 8. Varinder K. Aggarwal of the University of Bristol devised (Chem. Commun. 2010, 267) a Pd catalyst for the cyclocarbonylation of an alkenyl aziridine 9 to give the β-lactam 10. Iain Coldham of the University of Sheffield used (J. Org. Chem. 2010, 75, 4069) the ligand they had developed to effect enantioselective allylation of the pyrrolidine derivative 11. The corrresponding piperidine worked as well. John P. Wolfe of the University of Michigan established (Organic Lett. 2010, 12, 2322) that the Pd-mediated cyclization of 13 to 15 could be effected with high diastereocontrol. Christopher G. Frost of the University of Bath optimized (Angew. Chem. Int. Ed. 2010, 49, 1825) the tandem Ru-mediated conjugate addition/cyclization of 16 to give 18 in high ee. Barry M. Trost of Stanford University extended (J. Am. Chem. Soc. 2010, 132, 8238) their studies of trimethylenemethane cycloaddition to the ketimine 19, leading to the substituted pyrrolidine 21 in high ee. Pher G. Andersson of Uppsala University optimized (J. Am. Chem. Soc. 2010, 132, 8880) an Ir catalyst for the enantioselective hydrogenation of readily prepared tetrahydropyridines such as 22. Min Shi of the Shanghai Institute of Organic Chemistry devised (J. Org. Chem. 2010, 75, 3935) a Pd catalyst for enantioselective conjugate addition to the prochiral pyridone 24. Xiaojun Huang of Roche Palo Alto prepared (Tetrahedron Lett. 2010, 51, 1554) the monoacid 26 by enantioselective methanolysis of the anhydride. Selective formylation of the ester led to the pyridone 27.