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The preparations of several new (pentamethylcyclopentadienyl)osmium(II) complexes from the osmium(III) compound (C5Me5)2Os2Br4 are described; among these are phosphine and alkene complexes of stoichiometry (C5Me5)OsL2Br and (C5Me5)OsL2H as well as the nitrosyl complex (C5Me5)Os(NO)Br2. Treatment of (C5Me5)2Os2Br4 with PPh3 in ethanol or PMe3 in dichloromethane affords the osmium(II) complexes (C5Me5)OsL2Br, where L = PPh3 or PMe3; the 1,5-cyclooctadiene complex (C5Me5)Os(cod)Br can be made similarly in ethanol. Treatment of either the PPh3 or cod complex with other tertiary phosphines in refluxing heptane affords several other compounds of this class:  (C5Me5)OsL2Br, where L = PEt3, 1/2 Me2PCH2PMe2, 1/2 Me2PCH2CH2PMe2, or 1/2 Ph2PCH2PPh2. These bromoosmium(II) species serve as excellent starting materials for the preparation of other osmium(II) complexes. For example, treatment with NaBH4 in ethanol or with NaOMe in methanol affords the hydrides (C5Me5)OsL2H, where L = PMe3, PEt3, PPh3, 1/2 cod, 1/2 Me2PCH2PMe2, 1/2 Me2PCH2CH2PMe2, or 1/2 Ph2PCH2PPh2. Interestingly, treatment of (C5Me5)Os(PMe3)2Br with NaBH4 in refluxing ethanol affords the dihydride cation [(C5Me5)Os(PMe3)2H2 +], which can be deprotonated with methyllithium in tetrahydrofuran to afford the electrically neutral hydride (C5Me5)Os(PMe3)2H. This hydride complex is expected to be one of the most basic transition metal complexes known. Finally, treatment of (C5Me5)2Os2Br4 with nitric oxide in dichloromethane yields the osmium(II) complex (C5Me5)Os(NO)Br2. IR, NMR, and mass spectra of the new complexes are described. A secondary 13C/12C isotope effect on the 31P NMR chemical shifts of ca. 0.025 ppm is noted in several compounds. Comparisons of these osmium(II) compounds with analogous ruthenium species suggests that the former have stronger metal−ligand bonds, are slower to undergo nucleophilic substitution reactions, and are stronger reducing agents.

Background Individual health behaviours are considered important risk factors for cardiometabolic diseases. These behaviours may be socially patterned by early exposure to social disadvantage, but few studies have prospectively tested this hypothesis empirically. Aim We investigated whether childhood social disadvantage was associated with likelihood of engaging in less healthy behaviours 40 years later. Subjects and Methods Prospective data were analysed from the New England Family Study, a 2005–2007 adult follow-up of a cohort initiated in 1959–1966 (n=565). Childhood social environment (birth-age 7) was assessed using a cumulative index of socioeconomic and family stability factors. Logistic regression models evaluated associations between social disadvantage and each health-related behaviour and obesity in adulthood. Results Relative to low disadvantage, higher disadvantage was associated with 3.6-fold greater odds of smoking (95% CI: 1.9, 7.0), 4.8-fold greater odds (in women only) of excess alcohol consumption (95% CI: 1.6, 14.2), and 2.7-fold greater odds of obesity (95% CI: 1.3, 5.5), but was not associated with unhealthy diet or physical inactivity. Conclusion These findings suggest childhood social disadvantage may contribute to adult cardiometabolic disease by predisposing children to adopt certain unhealthy behaviours. If replicated, such findings may support intervention strategies that target social environmental factors and behavioural pathways that are established early in life.