Purpose The aim of this study was to investigate the association of femoral (FT), tibial (TT), and knee torsion (KT) on the patella tilt (PT), the axial engagement index (AEI), and the tibial tuberosity-trochlear groove distance (TTTG). Methods Femoral torsion, tibial torsion, knee torsion, patella tilt, the axial engagement index, the TTTG, and trochlear dysplasia were retrospectively evaluated on 59 patients suffering from recurrent patella instability or anterior knee pain with 118 torsional lower limb magnetic resonance imaging studies. Results FT and TT did not show any significant associations with TTTG, PT, and AEI (n.s.). KT was significantly associated with a higher TTTG, higher PT, and lower AEI (all, p < 0.001). Higher grade trochlear dysplasia was associated with a higher PT and lower AEI (both, p < 0.001). The Dejour classification showed no significant association with FT, TT, KT, and TTTG (n.s.). All measurement parameters showed an excellent interrater agreement (ICC 0.89-0.97). Conclusions Static patella tilt and patellofemoral axial engagement in knee extension are mainly influenced by knee torsion, TTTG, and trochlear dysplasia but not by femoral or tibial torsion. These findings help to understand the underlying reasons for the patella position in knee extensions in CT and MRI investigations in patients suffering from patella instability and patellofemoral pain syndrome. Level of evidence III.

Serum IGF-I is a well-established pharmacodynamic marker of GH administration in humans and has been used for this purpose in animal studies. However, its general suitability in wild-type laboratory mice has not been demonstrated. Here we show that treatment with recombinant human GH (rhGH) in four different strains of laboratory mice increases body weight, lean body mass, and liver weight but does not increase hepatic expression and release of IGF-I. In contrast and as expected, hypophysectomized rats show a rapid increase in serum IGF-I after rhGH administration. The lack of IGF-I up-regulation in mice occurs despite hepatic activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway and is not explained by GH dose, route of administration, origin of GH (i.e. recombinant human, bovine, and murine GH), treatment duration, genetic background, sex, or formation of neutralizing antibodies. Effects on other components of the GH/IGF pathway were highly influenced by genetic background and sex but not consistently affected by rhGH treatment. We conclude that IGF-I is not a reliable indicator of the biological effects of exogenous GH treatment in genetically and pharmacologically unmodified mice. We speculate that IGF-I release is already maximal in these animals and cannot be further increased by exogenous GH treatment. This is also suggested by the observation of restored IGF-I up-regulation in isolated murine hepatocytes after rhGH treatment. Total body weight, lean body mass, and liver weight may be more reliable phenotypic indicators in these models.

Overactivation of the complement system has been characterized in severe COVID-19 cases. Complement components are known to trigger NETosis via the coagulation cascade and have also been reported in human tracheobronchial epithelial cells. In this longitudinal study, we investigated systemic and local complement activation and NETosis in COVID-19 patients that underwent mechanical ventilation. Results confirmed significantly higher baseline levels of serum C5a (24.5 ± 39.0 ng/mL) and TCC (11.03 ± 8.52 µg/mL) in patients compared to healthy controls (p < 0.01 and p < 0.0001, respectively). Furthermore, systemic NETosis was significantly augmented in patients (5.87 (±3.71) × 106 neutrophils/mL) compared to healthy controls (0.82 (±0.74) × 106 neutrophils/mL) (p < 0.0001). In tracheal fluid, baseline TCC levels but not C5a and NETosis, were significantly higher in patients. Kinetic studies of systemic complement activation revealed markedly higher levels of TCC and CRP in nonsurvivors compared to survivors. In contrast, kinetic studies showed decreased local NETosis in tracheal fluid but comparable local complement activation in nonsurvivors compared to survivors. Systemic TCC and NETosis were significantly correlated with inflammation and coagulation markers. We propose that a ratio comprising systemic inflammation, complement activation, and chest X-ray score could be rendered as a predictive parameter of patient outcome in severe SARS-CoV-2 infections.