In situ formed Li/Cl phosphinidenoid complexes [Li(12-crown-4)][M(CO)5(ClPC5Me5)] 3a-c (M = Cr, Mo, W) reacted with cyclobutanone (4), cyclopentanone (5) and cyclohexanone (6) in Et2O to yield the first P-C5Me5 substituted C(3)-spirofused oxaphosphirane complexes 7a-c, 8a and 9a,a'. In the case of cyclopentanone and 1a the outcome of the reaction in THF was different: here the formation of 8a along with (anionic) phosphinoate complexes 14a and 15a was observed, the latter possess an unusual ring-opened oxaphosphirane and 2-cyclopentylidenecyclopentanone as co-ligands to the lithium cation. NMR, IR and MS data as well as single-crystal X-ray structures in the case of 7a-c, 8a, 9a and 15a are reported. DFT calculations on the parent 1-oxa-2-phosphaspiro[2.n]alkane pentacarbonylchromium(0) complexes 10 (a: n = 2; b: n = 3; c: n = 4; d: n = 5) revealed that both ring strain energies and G(r) values decrease significantly as the spiroring size increases. This is caused by an increase in the exocyclic α bond angle at the oxaphosphirane C(3) atom, hence decreasing the s-character of the corresponding orbitals involved in endocyclic bonds at C(3) and thus becoming better suited for accommodation of small ring angles.

Contentsp.2 Crystal data for 1a,b p.3 Crystal structure determination and molecular structure of 1a (Figure S1) p.4 Crystal structure determination and molecular structure of 1b (Figure S2)

Synthesis of the first oxaphosphirane chromium(0) and molybdenum(0) complexes of the type [{(R(1)PCH(R(2))-O}M(CO)(5)] (R(1) = C(5)Me(5)) (8a-e, 15a-e) and (R(1) = CH(SiMe(3))(2)) (9a-e, 16a-e) via reaction of dichloro(organo)- (1, 2, 10, 11) and chloro(organo)phosphane complexes (3,4,12) with lithium bases and aldehydes 7a-e is reported. Furthermore, bicyclic 1,3-oxaphospholane complexes 17 and 18 have been obtained via O-protonation of oxaphosphirane complexes 8a and 15a with HCl. All complexes were characterized by NMR, IR spectroscopic, mass spectrometric investigations and, in addition, single-crystal X-ray structures of complexes 8a-e, 9a,c, 15a,b,e, 16a-c, 17, 18 are presented and discussed.

Numerous studies on experimental ischemic stroke use the filament middle cerebral artery occlusion (fMCAo) model in C57BL/6 mice, but lesion sizes in this strain are highly variable. A known contributor is variation in the posterior communicating artery (PcomA) patency. We therefore aimed to provide a semiquantitative non-invasive in vivo method to routinely assess PcomA patency. We included 43 male C57BL/6 mice from four independent studies using a transient 45 min fMCAo model. Edema-corrected lesion sizes were measured by magnetic resonance (MR) imaging 24 h after reperfusion. Timeof-flight MR angiography was performed 7 days before and 24 h after fMCAo. Scores of PcomA size measured 24 h after, but not scores measured 7 days before fMCAo were negatively correlated with lesion size. Variability in PcomA patency explained 30% of the variance in our cohort (p < 0.0001, coefficient of determination r 2 = 0.3). In a simulation using parameters typical for experimental stroke research, the power to detect a true effect of d = 1 between two groups increased by 15% when an according covariate was included in the statistical model. We have demonstrated that in vivo measurement of PcomA size is feasible and can lead to increased accuracy in assessing the effect of treatments.