Shorter alkyl chains enhance molecular diffusion and electron transfer kinetics between photosensitisers and catalysts in CO2-reducing photocatalytic liposomes

Covalent functionalisation with alkyl tails is a common method for supporting molecular catalysts and photosensitisers onto lipid bilayers, but the influence of the alkyl chain length on the photocatalytic performances of the resulting liposomes is not well understood. In this work, we first prepared a series of rhenium-based CO2-reduction catalysts [Re(4,4'-(CnH2n+1)(2)-bpy)(CO)(3)Cl] (ReCn; 4,4'-(CnH2n+1)(2)-bpy=4,4'-dialkyl-2,2'-bipyridine) and ruthenium-based photosensitisers [Ru(bpy)(2)(4,4'-(CnH2n+1)(2)-bpy)](PF6)(2) (RuCn) with different alkyl chain lengths (n=0, 9, 12, 15, 17, and 19). We then prepared a series of PEGylated DPPC liposomes containing RuCn and ReCn, hereafter noted C-n, to perform photocatalytic CO2 reduction in the presence of sodium ascorbate. The photocatalytic performance of the C-n liposomes was found to depend on the alkyl tail length, as the turnover number for CO (TON) was inversely correlated to the alkyl chain length, with a more than fivefold higher CO production (TON=14.5) for the C-9 liposomes, compared to C-19 (TON=2.8). Based on immobilisation efficiency quantification, diffusion kinetics, and time-resolved spectroscopy, we identified the main reason for this trend: two types of membrane-bound RuCn species can be found in the membrane, either deeply buried in the bilayer and diffusing slowly, or less buried with much faster diffusion kinetics. Our data suggest that the higher photocatalytic performance of the C-9 system is due to the higher fraction of the more mobile and less buried molecular species, which leads to enhanced electron transfer kinetics between RuC9 and ReC9.Metals in Catalysis, Biomimetics & Inorganic Material

Directing the selectivity of oxygen reduction to water by confining a Cu catalyst in a metal organic framework

NWO739.017.003Metals in Catalysis, Biomimetics & Inorganic Material

Gonadal function in male and female patients with classic galactosemia

BACKGROUND: Hypergonadotropic hypoestrogenic infertility is the most burdensome complication for females suffering from classic galactosemia. In contrast, male gonadal function seems less affected. The underlying mechanism is not understood and several pathogenic mechanisms have been proposed. Timing of the lesion, prenatal or chronic post-natal, or a combination of both are not yet clear. METHODS: This review focuses on gonadal function in males and females, ovarian imaging and histology in this disease. It is based on the literature known to the authors and a Pubmed search using the keywords galactosemia, GALT deficiency, (premature) ovarian failure/insufficiency/dysfunction, testicular function, gonadotrophins, FSH, LH (published between January 1971 and April 2009). RESULTS: Male gonads are less affected, boys spontaneously reach puberty, although onset can be delayed. Semen quality has not been extensively studied. Several affected males are known to have fathered a child. Female gonads are invariably affected, although to a varied extent (hypergonadotropic hypoestrogenic ovarian dysfunction). Intriguingly, FSH is often already increased in infancy. Imaging usually shows hypoplastic and streak-like ovaries. Histological findings in some cases reveal the presence of morphologically normal but decreased numbers of primordial follicles, with the absence of intermediate and Graafian follicles. CONCLUSION: Gonads in males seem less affected than in females who exhibit hypergonadotropic hypoestrogenic subfertility. FSH can be elevated in infancy, and ovarian histology sometimes shows the presence of normal primordial follicles with absence of intermediate and Graafian follicles. These findings are similar to other genetic diseases primarily affecting the ovary

Gonadal function in male and female patients with classic galactosemia

Hypergonadotropic hypoestrogenic infertility is the most burdensome complication for females suffering from classic galactosemia. In contrast, male gonadal function seems less affected. The underlying mechanism is not understood and several pathogenic mechanisms have been proposed. Timing of the lesion, prenatal or chronic post-natal, or a combination of both are not yet clear. This review focuses on gonadal function in males and females, ovarian imaging and histology in this disease. It is based on the literature known to the authors and a Pubmed search using the keywords galactosemia, GALT deficiency, (premature) ovarian failure/insufficiency/dysfunction, testicular function, gonadotrophins, FSH, LH (published between January 1971 and April 2009). Male gonads are less affected, boys spontaneously reach puberty, although onset can be delayed. Semen quality has not been extensively studied. Several affected males are known to have fathered a child. Female gonads are invariably affected, although to a varied extent (hypergonadotropic hypoestrogenic ovarian dysfunction). Intriguingly, FSH is often already increased in infancy. Imaging usually shows hypoplastic and streak-like ovaries. Histological findings in some cases reveal the presence of morphologically normal but decreased numbers of primordial follicles, with the absence of intermediate and Graafian follicles. Gonads in males seem less affected than in females who exhibit hypergonadotropic hypoestrogenic subfertility. FSH can be elevated in infancy, and ovarian histology sometimes shows the presence of normal primordial follicles with absence of intermediate and Graafian follicles. These findings are similar to other genetic diseases primarily affecting the ovary