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Arno Kerling,1 Dagmar Hartung,2 Brendon Stubbs,3,4 Momme Kück,1 Uwe Tegtbur,1 Lena Grams,1 Thomas Sanjay Weber-Spickschen,1 Kai G Kahl5 1Institute of Sport Medicine, Hannover Medical School, Hannover, Germany; 2Institute for Diagnostic and Interventional Radiology, Hannover Medical School, Hannover, Germany; 3Physiotherapy Department, South London and Maudsley NHS Foundation Trust, Denmark Hill, London, UK; 4Health Service and Population Research Department, Institute of Psychiatry, King’s College London, London, UK; 5Department of Psychiatry, Social Psychiatry and Psychotherapy, Hannover Medical School, Hannover, Germany Objective: Sarcopenia leads to physical function impairment and at least to increasing all-cause mortality. There are notes on reduced muscle mass in patients with major depressive disorder (MDD). Whether an exercise intervention counteracts low muscle mass in patients with MDD has not been studied so far. Therefore, our study aimed at examining effects of regular aerobic exercise training on muscle mass in patients with MDD. Participants and methods: Thirty inpatients with MDD were included in the study, of which 20 received an additional supervised exercise program. Ten patients obtained treatment as usual. Muscle mass was measured using MRI before and 6 weeks after the training period (3 times per week for 45 minutes). Results: We found a significant effect of the exercise intervention on the amount of muscle mass depending on age, body mass index, and the physical activity score (P=0.042). Conclusion: Among other positive effects, regular exercise increases muscle mass in patients with MDD and, therefore, should be recommended as an additional treatment tool. Keywords: muscle mass, depression, sarcopenia, aerobic exercise

Although apoptosis within atherosclerotic plaques is associated with plaque vulnerability and rupture, the role of inhibition of the apoptotic process is not clear. We evaluated the impact of dietary modification and statin therapy (measures known to favorably influence outcomes in coronary disease) on the incidence of apoptosis in experimental atherosclerotic lesions. Methods: A total of 30 animals were studied; 1 group of 6 animals served as the controls (group 1), and the remaining 24 animals were subjected to balloon de-endothelialization of the abdominal aorta and a high-cholesterol diet. These atherosclerotic animals were randomized as follows: high-cholesterol diet for 4 mo (n = 6; untreated atherosclerotic group [group 2]), high-cholesterol diet for 3 mo and normal chow diet for 1 mo (n = 6; diet withdrawal group [group 3]), and high-cholesterol diet for 4 mo and simvastatin orally every day of the last month (n = 6; statin therapy group [group 4]). Tc-99m-Annexin A5 was used for noninvasive detection of apoptosis in groups 1-4. The remaining 6 rabbits on a high-cholesterol diet for 4 mo were studied with radiolabeled mutant annexin A5 (n = 6; nonspecific control group [group 51). Quantitative annexin A5 uptake in the abdominal aorta was determined and compared with the histologic and immunohistochemical characteristics of the atherosclerotic lesions. Results: Maximum annexin A5 uptake (mean +/- SD, 0.051 +/- 0.009 percentage injected dose per gram [%ID/g] of tissue) was observed in the untreated atherosclerotic animals. The uptake was substantially reduced in the diet withdrawal (0.03 +/- 0.006 %ID/g; P < 0.0001) and statin therapy (0.03 +/- 0.006 %ID/g; P < 0.0001) groups. The plaques in the untreated high-cholesterol group demonstrated advanced atherosclerotic lesions. On the other hand, the diet withdrawal and statin therapy groups showed histologic characteristics of stabilization, including the resolution of macrophage infiltration and an increase in smooth muscle cell content. There was a marked reduction in the apoptosis of macrophages. No significant uptake of annexin A5 or mutant annexin A5 was seen in rabbits on the normal chow diet or atherosclerotic rabbits, respectively. Conclusion: Dietary modification and statin therapy in atherosclerosis lead to a reduction in apoptosis and contribute to plaque stabilization. It can be hypothesized that a reduction in apoptosis is a favorable process in atherosclerotic disease.

Two series of SnO thin films, one doped with N and one doped with H, were deposited on c-plane sapphire by reactive ion beam sputter deposition starting from growth parameters optimized for stoichiometric SnO. The amounts of dopants incorporated into the SnO:H and SnO:N samples were quantified by secondary ion mass spectroscopy. The influence on the structural and electrical properties of SnO thin films was studied as a function of dopant concentration. In the case of N doping, all N incorporated, probably as N O , are active as the acceptor and exhibit long-term stability. We assign an acceptor activation energy of 100 to 150 meV to N O . However, we observe a change in the film morphology at a critical N concentration of about 7 ⋅ 10 17 cm − 3 , which deteriorates the structural properties of the films. In the case of SnO:H, the situation is different. We observe an outdiffusion of H after growth, i.e., the samples are not stable in the long term. Nevertheless, all H incorporated up to a H-content of 10 19 cm − 3 seem to be electrically active and exhibit an activation energy between 150 and 250 meV, likely corresponding to H i . Furthermore, at H contents above 10 19 cm − 3 , we observe molecular H 2 inside the SnO:H thin films. We conclude that N doping of SnO is better suited for tuning the p-type conductivity of SnO. However, it will be essential to overcome the morphology change observed at the critical N concentration to fully explore the tunability of the p-type conductivity in device applications. [ABSTRACT FROM AUTHOR]