[Internship-test reveals increased knowledge gaps]. / AT-provet avslöjar ökade kunskapsklyftor - Drygt 40 procent av AT-läkare med examen utanför EU underkänns - knappt 4 procent av dem med svensk examen.

We present the results of the medical knowledge test after fulfilled internship for Swedish medical authorization during the years 2009 to the spring of 2015. A total of 7,613 tests were analyzed. Interns graduated from Swedish universities failed in 2.7% to 3.8% of the test moments. Interns who graduated from countries within the European Union (EU) failed in 21.2% and interns graduated from a non-EU country failed in 41.6%. The results from those who graduated from EU and non-EU countries have worsened compared to an earlier study in 2009. Proper measures have now to be implemented for doctors graduated from a non-Swedish university to improve the outcome and introduction to the Swedish health care system.

Covered California: The Impact of Provider and Health Plan Market Power on Premiums.

We explain the establishment of Covered California, California's health insurance marketplace. The marketplace uses an active purchaser model, which means that Covered California can selectively contract with some health plans and exclude others. During the 2014 open-enrollment period, it enrolled 1.3 million people, who are covered by eleven health plans. We describe the market shares of health plans in California and in each of the nineteen rating regions. We examine the empirical relationship between measures of provider market concentration--spanning health plans, hospitals, and medical groups--and rating region premiums. To do this, we analyze premiums for silver and bronze plans for specific age groups. We find both medical group concentration and hospital concentration to be positively associated with premiums, while health plan concentration is not statistically significant. We simulate the impact of reducing hospital concentration to levels that would exist in moderately competitive markets. This produces a predicted overall premium reduction of more than 2 percent. However, in three of the nineteen rating regions, the predicted premium reduction was more than 10 percent. These results suggest the importance of provider market concentration on premiums.

Reduction of S-nitrosoglutathione by alcohol dehydrogenase 3 is facilitated by substrate alcohols via direct cofactor recycling and leads to GSH-controlled formation of glutathione transferase inhibitors.

GSNO (S-nitrosoglutathione) is emerging as a key regulator in NO signalling as it is in equilibrium with S-nitrosated proteins. Accordingly, it is of great interest to investigate GSNO metabolism in terms of competitive pathways and redox state. The present study explored ADH3 (alcohol dehydrogenase 3) in its dual function as GSNOR (GSNO reductase) and glutathione-dependent formaldehyde dehydrogenase. The glutathione adduct of formaldehyde, HMGSH (S-hydroxymethylglutathione), was oxidized with a k(cat)/K(m) value approx. 10 times the k(cat)/K(m) value of GSNO reduction, as determined by fluorescence spectroscopy. HMGSH oxidation in vitro was greatly accelerated in the presence of GSNO, which was concurrently reduced under cofactor recycling. Hence, considering the high cytosolic NAD(+)/NADH ratio, formaldehyde probably triggers ADH3-mediated GSNO reduction by enzyme-bound cofactor recycling and might result in a decrease in cellular S-NO (S-nitrosothiol) content in vivo. Formaldehyde exposure affected S-NO content in cultured cells with a trend towards decreased levels at concentrations of 1-5 mM, in agreement with the proposed mechanism. Product formation after GSNO reduction to the intermediate semimercaptal responded to GSH/GSNO ratios; ratios up to 2-fold allowed the spontaneous rearrangement to glutathione sulfinamide, whereas 5-fold excess of GSH favoured the interception of the intermediate to form glutathione disulfide. The sulfinamide and its hydrolysis product, glutathione sulfinic acid, inhibited GST (glutathione transferase) activity. Taken together, the findings of the present study provide indirect evidence for formaldehyde as a physiological trigger of GSNO depletion and show that GSNO reduction can result in the formation of GST inhibitors, which, however, is prevented under normal cellular redox conditions.