Operating Different Displays in Military Fast Jets Using Eye Gaze Tracker

This paper investigated the use of an eye-gaze-controlled interface in a military aviation environment. We set up a flight simulator and used the gaze-controlled interface in three different configurations of displays (head down, head up, and head mounted) for military fast jets. Our studies found that the gaze-controlled interface statistically significantly increased the speed of interaction for secondary mission control tasks compared to touchscreen- and joystick-based target designation system. Finally, we tested a gaze-controlled system inside an aircraft both on the ground and in different phases of flight with military pilots. Results showed that they could undertake representative pointing and selection tasks in less than two seconds, on average

Estimating pilots’ cognitive load from ocular parameters through simulation and in-flight studies

Eye tracking is the process of measuring either the point of gaze (where one is looking) or the motion of an eye relative to the head. This paper investigated use of eye gaze trackers in military aviation environment to automatically estimate pilot’s cognitive load from ocular parameters. We used a fixed base variable stability flight simulator with longitudinal tracking task and collected data from 14 military pilots. In a second study, we undertook three test flights with a BAES Hawk Trainer aircraft doing air to ground attack training missions and constant G level turn maneuvers up to +5G. Our study found that ocular parameters like rate of fixation is significantly different in different flying conditions and significantly correlate with altitude gradient during air to ground dive training task, normal load factor (G) of the aircraft during constant G level turn maneuvers and pilot’s control inceptor and tracking error in simulation tasks. Results from our studies can be used for real time estimation of pilots’ cognitive load, providing suitable warnings and alerts to the pilot in cockpit and training of military pilots on cognitive load management during operational missions

Educational Case: Mantle Cell Lymphoma

The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040

Pathophysiology of acute experimental pancreatitis: Lessons from genetically engineered animal models and new molecular approaches

The incidence of acute pancreatitis is growing and worldwide population-based studies report a doubling or tripling since the 1970s. 25% of acute pancreatitis are severe and associated with histological changes of necrotizing pancreatitis. There is still no specific medical treatment for acute pancreatitis. The average mortality resides around 10%. In order to develop new specific medical treatment strategies for acute pancreatitis, a better understanding of the pathophysiology during the onset of acute pancreatitis is necessary. Since it is difficult to study the early acinar events in human pancreatitis, several animal models of acute pancreatitis have been developed. By this, it is hoped that clues into human pathophysiology become possible. In the last decade, while employing molecular biology techniques, a major progress has been made. The genome of the mouse was recently sequenced. Various strategies are possible to prove a causal effect of a single gene or protein, using either gain-of-function (i.e., overexpression of the protein of interest) or loss-of-function studies (i.e., genetic deletion of the gene of interest). The availability of transgenic mouse models and gene deletion studies has clearly increased our knowledge about the pathophysiology of acute pancreatitis and enables us to study and confirm in vitro findings in animal models. In addition, transgenic models with specific genetic deletion or overexpression of genes help in understanding the role of one specific protein in a cascade of inflammatory processes such as pancreatitis where different proteins interact and co-react. This review summarizes the recent progress in this field. Copyright (c) 2005 S. Karger AG, Basel

The University of California San Francisco, Brain Metastases Stereotactic Radiosurgery (UCSF-BMSR) MRI Dataset

The University of California San Francisco Brain Metastases Stereotactic Radiosurgery (UCSF-BMSR) dataset is a public, clinical, multimodal brain MRI dataset consisting of 560 brain MRIs from 412 patients with expert annotations of 5136 brain metastases. Data consists of registered and skull stripped T1 post-contrast, T1 pre-contrast, FLAIR and subtraction (T1 pre-contrast - T1 post-contrast) images and voxelwise segmentations of enhancing brain metastases in NifTI format. The dataset also includes patient demographics, surgical status and primary cancer types. The UCSF-BSMR has been made publicly available in the hopes that researchers will use these data to push the boundaries of AI applications for brain metastases.Comment: 15 pages, 2 tables, 2 figure

Acute cholecystitis with massive upper gastrointestinal bleed: A case report and review of the literature

BACKGROUND: Cystic artery pseudoaneurysm is a rare complication following cholecystitis. Its presentation with upper gastrointestinal hemorrhage (UGIH) is even rarer. Thirteen patients with cystic artery pseudoaneurysm have been reported in the literature but only 2 of them presented with UGIH alone. CASE PRESENTATION: We report a 43-year-old woman who developed a cystic artery pseudoaneurysm following an episode of acute cholecystitis. She presented with haematemesis and melaena associated with postural symptoms. Upper gastrointestinal endoscopy revealed a duodenal ulcer with adherent clots in the first part of the duodenum. Ultrasonography detected gallstones and a pseudoaneurysm at the porta hepatis. Selective hepatic angiography showed two small pseudoaneurysms in relation to the cystic artery, which were selectively embolized. However, the patient developed abdominal signs suggestive of gangrene of the gall bladder and underwent an emergency laparotomy. Cholecystectomy with common bile duct exploration along with repair of the duodenal rent, and pyloric exclusion and gastrojejunostomy was done. CONCLUSION: This case illustrates the occurrence of a rare complication (pseudoaneurysm) following cholecystitis with an unusual presentation (UGIH). Cholecystectomy, ligation of the pseudoaneurysm and repair of the intestinal communication is an effective modality of treatment

Inhibitors of Bcl-2 protein family deplete ER Ca2+ stores in pancreatic acinar cells

Physiological stimulation of pancreatic acinar cells by cholecystokinin and acetylcholine activate a spatial-temporal pattern of cytosolic [Ca+2] changes that are regulated by a coordinated response of inositol 1,4,5-trisphosphate receptors (IP3Rs), ryanodine receptors (RyRs) and calcium-induced calcium release (CICR). For the present study, we designed experiments to determine the potential role of Bcl-2 proteins in these patterns of cytosolic [Ca+2] responses. We used small molecule inhibitors that disrupt the interactions between prosurvival Bcl-2 proteins (i.e. Bcl-2 and Bcl-xl) and proapoptotic Bcl-2 proteins (i.e. Bax) and fluorescence microfluorimetry techniques to measure both cytosolic [Ca+2] and endoplasmic reticulum [Ca+2]. We found that the inhibitors of Bcl-2 protein interactions caused a slow and complete release of intracellular agonist-sensitive stores of calcium. The release was attenuated by inhibitors of IP3Rs and RyRs and substantially reduced by strong [Ca2+] buffering. Inhibition of IP3Rs and RyRs also dramatically reduced activation of apoptosis by BH3I-2′. CICR induced by different doses of BH3I-2′ in Bcl-2 overexpressing cells was markedly decreased compared with control. The results suggest that Bcl-2 proteins regulate calcium release from the intracellular stores and suggest that the spatial-temporal patterns of agonist-stimulated cytosolic [Ca+2] changes are regulated by differential cellular distribution of interacting pairs of prosurvival and proapoptotic Bcl-2 proteins