Synthesis of Rh(iii) thiophosphinito pincer hydrido complexes by base-free C-H bond activation at room temperature.

Rhodium(iii) thiophosphinito pincer hydrido complexes were synthesised by C-H activation under exceptionally mild conditions at room temperature without additional base or irradiation and fully characterised by multinuclear NMR spectroscopy and X-ray crystallography. C-H activation under these mild conditions contrasts with the reactivity of related systems with POCOP ligands.

Iridium(iii) hydrido complexes for the catalytic dehydrogenation of hydrazine borane.

The synthesis of 3,5-disubstituted cyclometalated iridium(iii) hydrido complexes of the type [3,5-R2(POCOP)IrHX] (3,5-R2(POCOP) = κ3-C5HR2-2,6-(OPtBu2)2 with R = t-Bu, COOMe; X = Cl, H) is described. All complexes were investigated in the catalytic dehydrogenation of hydrazine borane and compared with the unsubstituted compounds [(POCOP)IrHX] (X = Cl, H). All catalysts are highly active and recyclable, clearly maintaining hydrogen production activity. The dehydrogenation products were structurally characterised by solid state NMR and FTIR spectroscopy. Experimental observations were complemented by a dispersion-corrected DFT study to rationalise the mechanism of hydrazine borane dehydrogenation.

Formation of trinuclear rhodium-hydride complexes [{Rh(PP*)H}3-(µ2-H)3(µ3-H)][anion]2--during asymmetric hydrogenation?

Recently described and fully characterized trinuclear rhodium-hydride complexes [{Rh(PP*)H}3(µ2-H)3(µ3-H)][anion]2 have been investigated with respect to their formation and role under the conditions of asymmetric hydrogenation. Catalyst-substrate complexes with mac (methyl (Z)-N-acetylaminocinnamate) ([Rh(tBu-BisP*)(mac)]BF4, [Rh(Tangphos)(mac)]BF4, [Rh(Me-BPE)(mac)]BF4, [Rh(DCPE)(mac)]BF4, [Rh(DCPB)(mac)]BF4), as well as rhodium-hydride species, both mono-([Rh(Tangphos)-H2(MeOH)2]BF4, [Rh(Me-BPE)H2(MeOH)2]BF4), and dinuclear ([{Rh(DCPE)H}2(µ2-H)3]BF4, [{Rh(DCPB)H}2(µ2-H)3]BF4), are described. A plausible reaction sequence for the formation of the trinuclear rhodium-hydride complexes is discussed. Evidence is provided that the presence of multinuclear rhodium-hydride complexes should be taken into account when discussing the mechanism of rhodium-promoted asymmetric hydrogenation.

Viral hepatitis in patients with spinal cord injury is explained by known risk factors.

Spinal cord injury (SCI) has been reported to be associated with viral hepatitis. However, this association may be related to other confounding factors, such as intravenous drug abuse or blood transfusions. Screening for viral hepatitis associated risk factors and serum serologies, including HBsAg, anti-HBc, anti-HBs and anti-HCV testing, were performed in 78 randomly selected SCI patients and 93 non-alcoholic patients attending a general medical clinic. Hepatitis B and C seropositivies in SCI patients were 29.5 percent and 14.1 percent, respectively, and were significantly associated with a history of intravenous drug abuse. In contrast, hepatitis B and C seropositivities in non-alcoholic general medicine clinic patients were 22.6 percent and 2.2 percent, respectively. In the subgroup of patients without known viral hepatitis risk factors, there were no significant differences between SCI and non-alcoholic patients with respect to hepatitis B (21.4 percent vs. 22.1 percent) or hepatitis C (0 percent vs. 1.3 percent) seropositivity. Stepwise logistic regression also failed to detect an association of SCI with viral hepatitis. In conclusion, the increased seroprevalence of hepatitis C in SCI patients is secondary to intravenous drug use and blood transfusions. Further preventive measures such as improved hepatitis screening of blood donors and substance abuse treatment should decrease viral hepatitis exposure in SCI patients.

Prevalence of viral hepatitis B in an urban veteran spinal cord injured population.

The objective of this study was to determine the prevalence of viral hepatitis B (HBV) seropositivity in an urban veteran population with spinal cord injury (SCI) and the relationship of liver function test (LFT) values to HBV seropositivity. Eighty patients with chronic SCI (44 inpatients and 36 outpatients) had liver function tests (LFTs), hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBsAb) and hepatitis B core antibody (anti-HBcAb) evaluated. Seventy-seven able-bodied (non-SCI) outpatients without known viral hepatitis risk factors served as an urban veteran reference group. Results demonstrated a high prevalence of seropositivity for HBV in both veteran groups (SCI = 29 percent; non-SCI = 22 percent). Subdividing the SCI group by inpatients and outpatients, HBV positivity was found to be significantly higher in the SCI inpatients than in either the SCI outpatient (39 percent vs 17 percent, x2 = 4.67, p < 0.05) or non-SCI groups (39 percent vs 22 percent, x2 = 3.80, p = 0.05). For the whole group, the gamma-glutamyl transpeptidase (GGT) level was greater in the HBV seropositive (n = 40) compared with the HBV seronegative (n = 117) populations (82 +/- 17 vs 46 +/- 7 U/L, p = 0.019, respectively). In addition, the subgroup of spinal cord patients seropositive for hepatitis B (n = 23) had a higher mean GGT than their seronegative (n = 57) counterparts (101 +/- 26 vs 47 +/- 9 U/L, p = 0.018, respectively). We conclude that urban veterans in general, and especially those inpatients with SCI, may be at increased risk of HBV infection. An HBV vaccination program for veteran patients with SCI may be warranted.