Background: The safety of performing spinal anaesthesia for both patients and anaesthetists alike in the presence of active infection with the novel coronavirus disease 2019 (COVID-19) is unclear. Here, we report the clinical characteristics and outcomes for both patients with COVID-19 and the anaesthetists who provided their spinal anaesthesia. Methods: Forty-nine patients with radiologically confirmed COVID-19 for Caesarean section or lower-limb surgery undergoing spinal anaesthesia in Zhongnan Hospital, Wuhan, China participated in this retrospective study. Clinical characteristics and perioperative outcomes were recorded. For anaesthesiologists exposed to patients with COVID-19 by providing spinal anaesthesia, the level of personal protective equipment (PPE) used, clinical outcomes (pulmonary CT scans), and confirmed COVID-19 transmission rates (polymerase chain reaction [PCR]) were reviewed. Results: Forty-nine patients with COVID-19 requiring supplementary oxygen before surgery had spinal anaesthesia (ropivacaine 0.75%), chiefly for Caesarean section (45/49 [91%]). Spinal anaesthesia was not associated with cardiorespiratory compromise intraoperatively. No patients subsequently developed severe pneumonia. Of 44 anaesthetists, 37 (84.1%) provided spinal anaesthesia using Level 3 PPE. Coronavirus disease 2019 infection was subsequently confirmed by PCR in 5/44 (11.4%) anaesthetists. One (2.7%) of 37 anaesthetists who wore Level 3 PPE developed PCR-confirmed COVID-19 compared with 4/7 (57.1%) anaesthetists who had Level 1 protection in the operating theatre (relative risk reduction: 95.3% [95% confidence intervals: 63.7e99.4]; P<0.01). Conclusions: Spinal anaesthesia was delivered safely in patients with active COVID-19 infection, the majority of whom had Caesarean sections. Level 3 PPE appears to reduce the risk of transmission to anaesthetists who are exposed to mildly symptomatic surgical patients.

The mechanical properties of elastin network from bovine thoracic aorta under biaxial tensile loading were studied both experimentally and theoretically. Histology and scanning electron microscopy were performed to verify the removal of cells, collagen, and other extracellular matrix components. Equi- and nonequi-biaxial tests were performed to study the effect of different loading conditions on the stress-strain responses of the elastin network. The mechanical properties of different elastin sections along the thoracic aorta were examined and studied to understand the anisotropy of elastin along the whole artery. Biaxial tensile test data comparing elastin vs. intact aorta showed that elastin is mainly responsible for the linear elastic response of the arterial wall at lower strains. Experimental results revealed that elastin network possesses significant anisotropic mechanical properties with the circumferential direction being stiffer than the longitudinal direction. The mechanical properties of elastin vary significantly along the thoracic aorta, with the thin section appearing to have the highest tangent modulus. Biological assay results indicate that elastin content is about the same along the thoracic aorta. The mechanical behavior of elastin network was well captured by the eight-chain statistical mechanics based microstructural model. Material parameters obtained from the equi-biaxial test were able to predict the stress-strain responses of elastin network under arbitrary nonequi-biaxial loading conditions. Also, by varying material parameters in the model, the changes in microstructure such as elastin fiber orientation and cross-linking density on the macroscopic mechanical properties of elastin network were discussed.

The abnormal self-assembly of amyloid-β (Aβ) peptides into toxic fibrillar aggregates is associated with the pathogenesis of Alzheimer’s disease (AD). The inhibition of β-sheet-rich oligomer formation is considered as the primary therapeutic strategy for AD. Previous experimental studies reported that norepinephrine (NE), one of the neurotransmitters, is able to inhibit Aβ aggregation and disaggregate the preformed fibrils. Moreover, exercise can markedly increase the level of NE. However, the underlying inhibitory and disruptive mechanisms remain elusive. In this work, we performed extensive replica-exchange molecular dynamic (REMD) simulations to investigate the conformational ensemble of Aβ1–42 dimer with and without NE molecules. Our results show that without NE molecules, Aβ1–42 dimer transiently adopts a β-hairpin-containing structure, and the β-strand regions of this β-hairpin (residues 15QK­LVFF­A21 and 33GL­MVGG­VV40) strongly resemble those of the Aβ fibril structure (residues 15QK­LVFF­A21 and 30AI­IGLM­VG37) reported in an electron paramagnetic resonance spectroscopy study. NE molecules greatly reduce the interpeptide β-sheet content and suppress the formation of the above-mentioned β-hairpin, leading to a more disordered coil-rich Aβ dimer. Five dominant binding sites are identified, and the central hydrophobic core 16KLV­FFA21 site and C-terminal 31II­GLM­V36 hydrophobic site are the two most favorable ones. Our data reveal that hydrophobic, aromatic stacking, hydrogen-bonding and cation-π interactions synergistically contribute to the binding of NE molecules to Aβ peptides. MD simulations of Aβ1–42 protofibril show that NE molecules destabilize Aβ protofibril by forming H-bonds with residues D1, A2, D23, and A42. This work reveals the molecular mechanism by which NE molecules inhibit Aβ1–42 aggregation and disaggregate Aβ protofibrils, providing valuable information for developing new drug candidates and exercise therapy against AD.

Background Decellularized tissues are expected to have major cellular immunogenic components removed and in the mean time maintain similar mechanical strength and extracellular matrix (ECM) structure. However, the decellularization processes likely cause alterations of the ECM structure and thus influence the mechanical properties. In the present study, the effects of different decellularization protocols on the (passive) mechanical properties of the resulted porcine aortic ECM were evaluated. Methods Decellularization methods using anionic detergent (sodium dodecyl sulfate), enzymatic detergent (Trypsin), and non-ionic detergent (tert-octylphenylpolyoxyethylen (Triton X-100)) were adopted to obtain decellularized porcine aortic ECM. Histological studies and scanning electron microscopy were performed to confirm the removal of cells and to examine the structure of ECM. Biaxial tensile testing was used to characterize both the elastic and viscoelastic mechanical behaviors of decellularized ECM. Results All three decellularization protocols remove the cells effectively. The major ECM structure is preserved under SDS and Triton X-100 treatments. However, the structure of Trypsin treated ECM is severely disrupted. SDS and Triton X-100 decellularized ECM exhibits similar elastic properties as intact aorta tissues. Decellularized ECM shows less stress relaxation than intact aorta due to the removal of cells. Creep behavior is negligible for both decellularized ECM and intact aortas. Conclusion SDS and Triton X-100 decellularized ECM tissue appeared to maintain the critical mechanical and structural properties and might work as a potential material for further vascular tissue engineering.

In this paper, we studied the viscoelastic behaviors of isolated aortic elastin using combined modeling and experimental approaches. Biaxial stress relaxation and creep experiments were performed to study the time-dependent behavior of elastin. Experimental results reveal that stress relaxation preconditioning is necessary in order to obtain repeatable stress relaxation responses. Elastin exhibits less stress relaxation than intact or decellularized aorta. The rate of stress relaxation of intact and decellularized aorta is linearly dependent on the initial stress levels. The rate of stress relaxation for elastin increases linearly at stress levels below about 60 kPa; however, the rate changes very slightly at higher initial stress levels. Experimental results also show that creep response is negligible for elastin, and the intact or decellularized aorta. A quasi-linear viscoelasticity model was incorporated into a statistical mechanics based eight-chain microstructural model at the fiber level to simulate the orthotropic viscoelastic behavior of elastin. A user material subroutine was developed for finite element analysis. Results demonstrate that this model is suitable to capture both the orthotropic hyperelasticity and viscoelasticity of elastin.