The influence of rotator cuff tear type and weight bearing on shoulder biomechanics in an ex vivo simulator experiment.

Glenohumeral biomechanics after rotator cuff (RC) tears have not been fully elucidated. This study aimed to investigate the muscle compensatory mechanism in weight-bearing shoulders with RC tears and asses the induced pathomechanics (i.e., glenohumeral translation, joint instability, center of force (CoF), joint reaction force). An experimental, glenohumeral simulator with muscle-mimicking cable system was used to simulate 30° scaption motion. Eight fresh-frozen shoulders were prepared and mounted in the simulator. Specimen-specific scapular anthropometry was used to test six RC tear types, with intact RC serving as the control, and three weight-bearing loads, with the non-weight-bearing condition serving as the control. Glenohumeral translation was calculated using instantaneous helical axis. CoF, muscle forces, and joint reaction forces were measured using force sensors integrated into the simulator. Linear mixed effects models (RC tear type and weight-bearing) with random effects (specimen and sex) were used to assess differences in glenohumeral biomechanics. RC tears did not change the glenohumeral translation (p > 0.05) but shifted the CoF superiorly (p ≤ 0.005). Glenohumeral translation and joint reaction forces increased with increasing weight bearing (p < 0.001). RC and deltoid muscle forces increased with the presence of RC tears (p ≤ 0.046) and increased weight bearing (p ≤ 0.042). The synergistic muscles compensated for the torn RC tendons, and the glenohumeral translation remained comparable to that for the intact RC tendons. However, in RC tears, the more superior CoF was close to where glenoid erosion occurs in RC tear patients with secondary osteoarthritis. These findings underscore the importance of early detection and precise management of RC tears.

On-chip generation and dynamic piezo-optomechanical rotation of single photons.

Integrated photonic circuits are key components for photonic quantum technologies and for the implementation of chip-based quantum devices. Future applications demand flexible architectures to overcome common limitations of many current devices, for instance the lack of tuneabilty or built-in quantum light sources. Here, we report on a dynamically reconfigurable integrated photonic circuit comprising integrated quantum dots (QDs), a Mach-Zehnder interferometer (MZI) and surface acoustic wave (SAW) transducers directly fabricated on a monolithic semiconductor platform. We demonstrate on-chip single photon generation by the QD and its sub-nanosecond dynamic on-chip control. Two independently applied SAWs piezo-optomechanically rotate the single photon in the MZI or spectrally modulate the QD emission wavelength. In the MZI, SAWs imprint a time-dependent optical phase and modulate the qubit rotation to the output superposition state. This enables dynamic single photon routing with frequencies exceeding one gigahertz. Finally, the combination of the dynamic single photon control and spectral tuning of the QD realizes wavelength multiplexing of the input photon state and demultiplexing it at the output. Our approach is scalable to multi-component integrated quantum photonic circuits and is compatible with hybrid photonic architectures and other key components for instance photonic resonators or on-chip detectors.

Effect of decompressive craniectomy on outcome following subarachnoid hemorrhage in mice.

BACKGROUND AND PURPOSE: Elevated intracranial pressure (ICP) is a key feature of subarachnoid hemorrhage (SAH). Here, we examined the role of elevated ICP in the pathophysiology of SAH, and we investigated whether decreasing ICP by performing decompressive craniectomy (DC) can improve outcome. METHODS: SAH was induced in male C57BL/6 mice via endovascular Circle of Willis perforation in the following 4 groups: sham surgery, SAH, DC after SAH, and DC before SAH. DC was performed either 15 minutes before or after SAH induction. ICP, cerebral blood flow, heart rate, oxygen saturation, and end-tidal PCO2 were monitored for 45 minutes. After surgery, neurological function was evaluated daily for 7 days. After killing, hippocampal neurons, corpus callosum thickness, and ventricular volume were evaluated on paraformaldehyde-fixed coronal brain sections. RESULTS: Although DC reduced SAH-induced ICP, it yielded no beneficial effect with respect to posthemorrhagic hypoperfusion; moreover, DC increased the incidence of rebleeding, induced more severe neurological impairments, and caused higher mortality. Post SAH, mice that survived 7 days had no histopathologic differences, regardless of whether DC was performed. CONCLUSIONS: Performing DC to reduce ICP either during or acutely after SAH resulted in more severe bleeding, a higher incidence of rebleeding, and poorer outcome. Thus, elevated post-hemorrhagic ICP plays an important role in controlling bleeding after SAH and should therefore not be reduced acutely. If DC is considered for treating a patient with SAH, the timing of decompression should take these effects into consideration.

Protocol for the induction of subarachnoid hemorrhage in mice by perforation of the Circle of Willis with an endovascular filament.

Genetically engineered mice are a valuable tool to investigate the molecular and cellular mechanisms leading to brain damage following subarachnoid hemorrhage (SAH). Therefore, several murine SAH models were developed during the last 15 years. Among those models, the perforation of the Circle of Willis by an endovascular filament or "filament model" turned out to become the most popular one, since it is believed to reproduce some of the most prominent pathophysiological features observed after human SAH. Despite the importance of the endovascular filament model for SAH research, relatively few studies were published using this technique during the past years and a number of laboratories reported problems establishing the technique. This triggered discussions about the standardization, reproducibility, and the reliability of the model. In order to improve this situation, the current paper aims to provide a comprehensive hands-on protocol of the murine endovascular filament model. The protocol proved to result in induction of SAH in mice with high intrapersonal and interpersonal reproducibility and is based on our experience with this technique for more than 10 years. By sharing our experience with this valuable model, we aim to initiate a constantly ongoing discussion process on the improvement of standards and techniques in the field of experimental SAH research.

A murine model of subarachnoid hemorrhage.

In this video publication a standardized mouse model of subarachnoid hemorrhage (SAH) is presented. Bleeding is induced by endovascular Circle of Willis perforation (CWp) and proven by intracranial pressure (ICP) monitoring. Thereby a homogenous blood distribution in subarachnoid spaces surrounding the arterial circulation and cerebellar fissures is achieved. Animal physiology is maintained by intubation, mechanical ventilation, and continuous on-line monitoring of various physiological and cardiovascular parameters: body temperature, systemic blood pressure, heart rate, and hemoglobin saturation. Thereby the cerebral perfusion pressure can be tightly monitored resulting in a less variable volume of extravasated blood. This allows a better standardization of endovascular filament perforation in mice and makes the whole model highly reproducible. Thus it is readily available for pharmacological and pathophysiological studies in wild type and genetically altered mice.