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Cage-chiral tetra-tert-butyl-P5-deltacyclene 5 is accessible as a pair of highly enriched enantiomers 5′ and 5′′. The only secondary phosphorus atom P1 of the cage can be selectively oxidized by reaction with t-BuOOH. The P1-oxo species 9a′ and 9a′′, allow the direct determination of their ee values. Oxidation occurs with the complete retention of the optical activity of the compounds. The chiroptical properties of 9a′ and 9a′′ are strongly dominated by their cage chirality, the oxygen atom does not contribute significantly. Elemental sulfur and selenium oxidize P5 with high preference to yield P5-thio- and P5-seleno-P5-deltacyclenes 10 and 11 of the intact cages again. Longer reaction time and more than stoichiometric amounts of selenium, leads to tri-seleno-P5-tetracycloundecane 12, a partially opened oxidized rearrangement product. The ligand properties of racemic 9a were determined. Diphosphetane phosphorus atom P2 of 9a is the active donor center to bind a Cr(CO)5 fragment, but a tautomerization of 9a takes place if [(benzene)RuCl2]2 is added. A hydrogen atom migrates from P1 to the oxygen atom to form a phosphinous acid ligand. The lone pair of P1 is regenerated and acts as the active ligand function of the cage in this case. As for 5, the base n-BuLi induces an efficient cage rearrangement reaction of 9a, where P1 and the neighboring carbon atom C4 containing its t-Bu substituent change places. C4 moves to its new position without breaking the bond with P5, this way forming the novel P1-oxo-P5-norsnoutene cage in a highly diastereoselective process. [ABSTRACT FROM AUTHOR]

Erectile dysfunction (ED) can impair the quality of life and the relationship. An early treatment is necessary to avoid the development of comorbid complaints. To arise the help-seeking behavior and to improve the treatment of affected men, it is necessary to be aware of the treatment expectations. The objective of this study was to investigate the treatment expectations of men with ED and their female partners. This is an explorative qualitative study using semistructured telephone interviews with 12 men with ED and their female partners. Interviews were tape-recorded, transcribed and analyzed on the basis of the grounded theory. We could identify various treatment expectations, which could be differentiated into expectations according to the conditions (for example, low costs and an early access), the handling of the practitioner (for example, showing interest and taking the patient seriously or incorporate the female partner), the treatment itself (for example, clearing the causes and helpful medication) and the treatment outcome (for example, having no ED and more sexual desire). Considering the identified expectations could increase treatment motivation and compliance. We derive five theses from our data, how to implement our findings. [ABSTRACT FROM AUTHOR]

BACKGROUND AND PURPOSE Haemorrhagic shock and resuscitation (H/R) induces hepatic injury, strong inflammatory changes and death. Alcohol intoxication is assumed to worsen pathophysiological derangements after H/R. Here, we studied the effects of acute alcohol intoxication on survival, liver injury and inflammation after H/R, in rats. EXPERIMENTAL APPROACH Rats were given a single oral dose of ethanol (5 g·kg−1, 30%) or saline (control), 12 h before they were haemorrhaged for 60 min and resuscitated (H/R). Sham groups received the same procedures without H/R. Measurements were made 2, 24 and 72 h after resuscitation. Survival was assessed 72 h after H/R. KEY RESULTS Ethanol increased survival after H/R three-fold and also induced fatty changes in the liver. H/R-induced liver injury was amplified by ethanol at 2 h but inhibited 24 h after H/R. Elevated serum IL-6 levels as well as hepatic IL-6 and TNF-α gene expression 2 h after H/R were reduced by ethanol. Ethanol enhanced serum IL-1β at 2 h, but did not affect increased hepatic IL-1β expression at 72 h after H/R. Local inflammatory markers, hepatic infiltration with polymorphonuclear leukocytes and intercellular adhesion molecule 1 expression decreased after ethanol compared with saline, following H/R. Ethanol reduced H/R-induced IκBα activation 2 h after H/R, and NF-κB-dependent gene expression of MMP9. CONCLUSIONS AND IMPLICATIONS Ethanol reduced H/R-induced mortality at 72 h, accompanied by a suppression of proinflammatory changes after H/R in ethanol-treated animals. Binge-like ethanol exposure modulated the inflammatory response after H/R, an effect that was associated with NF-κB activity. [ABSTRACT FROM AUTHOR]