Characterization of Silicon Crystals Grown from Melt in a Granulate Crucible

The growth of silicon crystals from a melt contained in a granulate crucible significantly differs from the classical growth techniques because of the granulate feedstock and the continuous growth process. We performed a systematic study of impurities and structural defects in several such crystals with diameters up to 60 mm. The possible origin of various defects is discussed and attributed to feedstock (concentration of transition metals), growth setup (carbon concentration), or growth process (dislocation density), showing the potential for further optimization. A distinct correlation between crystal defects and bulk carrier lifetime is observed. A bulk carrier lifetime with values up to 600 μs on passivated surfaces of dislocation-free parts of the crystal is currently achieved

Rekonstruktion großer osteochondraler Defekte des distalen Femurs und der proximalen Tibia

The reconstruction of large osteochondral defects is still a challenge in musculoskeletal surgery. Fresh frozen allografts are a frequently used resource for the treatment of such tissue defects. Furthermore, 3D-printed models enable multiple options in the preoperative planning and intraoperative adaptation of the allografts, so that healing is optimal and the best functional outcome for the patient is achieved.Die Rekonstruktion großer osteochondraler Defekte stellt nach wie vor eine Herausforderung in der muskuloskeletalen Chirurgie dar. Frisch gefrorene Allografts sind eine häufig genutzte Ressource für die Behandlung solcher Gewebedefekte. Darüber hinaus ermöglichen 3D-gedruckte Kunststoffmodelle vielfältige Optionen in der präoperativen Planung und bei der intraoperativen Anpassung der Transplantate, sodass sie optimal einheilen und das bestmögliche funktionelle Ergebnis für den Patienten erreicht wird

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council

Stabilisation of RNA bulges by oligonucleotide complements containing an adenosine analogue

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