Reducing flight upset risk and startle response: A study of the wake vortex alert with licensed commercial pilots.

The study aimed at investigating the impact of an innovative Wake Vortex Alert (WVA) avionics on pilots' operation and mental states, intending to improve aviation safety by mitigating the risks associated with wake vortex encounters (WVEs). Wake vortices, generated by jet aircraft, pose a significant hazard to trailing or crossing aircrafts. Despite existing separation rules, incidents involving WVEs continue to occur, especially affecting smaller aircrafts like business jets, resulting in aircraft upsets and occasional cabin injuries. To address these challenges, the study focused on developing and validating an alert system that can be presented to air traffic controllers, enabling them to warn flight crews. This empowers the flight crews to either avoid the wake vortex or secure the cabin to prevent injuries. The research employed a multidimensional approach including an analysis of human performance and human factors (HF) issues to determine the potential impact of the alert on pilots' roles, tasks, and mental states. It also utilizes Human Assurance Levels (HALs) to evaluate the necessary human factors support based on the safety criticality of the new system. Realistic flight simulations were conducted to collect data of pilots' behavioural, subjective and neurophysiological responses during WVEs. The data allowed for an objective evaluation of the WVA impact on pilots' operation, behaviour and mental states (mental workload, stress levels and arousal). In particular, the results highlighted the effectiveness of the alert system in facilitating pilots' preparation, awareness and crew resource management (CRM). The results also highlighted the importance of avionics able to enhance aviation safety and reducing risks associated with wake vortex encounters. In particular, we demonstrated how providing timely information and improving situational awareness, the WVA will minimize the occurrence of WVEs and contribute to safer aviation operations.

Regional Anesthesia Techniques for Shoulder Surgery in High-Risk Pulmonary Patients.

Patients with pre-existing pulmonary conditions are at risk for experiencing perioperative complications and increased morbidity. General anesthesia has historically been used for shoulder surgery, though regional anesthesia techniques are increasingly used to provide anesthesia and improved pain control after surgery. Relative to regional anesthesia, patients who undergo general anesthesia may be more prone to risks of barotrauma, postoperative hypoxemia, and pneumonia. High-risk pulmonary patients, in particular, may be exposed to these risks of general anesthesia. Traditional regional anesthesia techniques for shoulder surgery are associated with high rates of phrenic nerve paralysis which significantly impairs pulmonary function. Newer regional anesthesia techniques have been developed, however, that provide effective analgesia and surgical anesthesia while having much lower rates of phrenic nerve paralysis, thereby preserving pulmonary function.

Loss of Coupling Distinguishes GJB1 Mutations Associated with CNS Manifestations of CMT1X from Those Without CNS Manifestations.

CMT1X, an X-linked inherited neuropathy, is caused by mutations in GJB1, which codes for Cx32, a gap junction protein expressed by Schwann cells and oligodendrocytes. Many GJB1 mutations cause central nervous system (CNS) abnormality in males, including stable subclinical signs and, less often, short-duration episodes characterized by motor difficulties and altered consciousness. However, some mutations have no apparent CNS effects. What distinguishes mutations with and without CNS manifestations has been unclear. Here we studied a total of 14 Cx32 mutations, 10 of which are associated with florid episodic CNS clinical syndromes in addition to peripheral neuropathy. The other 4 mutations exhibit neuropathy without clinical or subclinical CNS abnormalities. These "PNS-only" mutations (Y151C, V181M, R183C and L239I) form gap junction plaques and produce levels of junctional coupling similar to those for wild-type Cx32. In contrast, mutants with CNS manifestations (F51L, E102del, V139M, R142Q, R142W, R164W T55I, R164Q and C168Y) either form no morphological gap junction plaques or, if they do, produce little or no detectable junctional coupling. Thus, PNS and CNS abnormalities may involve different aspects of connexin function.