An auditory-visual tradeoff in susceptibility to clutter.

Sensory cortical mechanisms combine auditory or visual features into perceived objects. This is difficult in noisy or cluttered environments. Knowing that individuals vary greatly in their susceptibility to clutter, we wondered whether there might be a relation between an individual's auditory and visual susceptibilities to clutter. In auditory masking, background sound makes spoken words unrecognizable. When masking arises due to interference at central auditory processing stages, beyond the cochlea, it is called informational masking. A strikingly similar phenomenon in vision, called visual crowding, occurs when nearby clutter makes a target object unrecognizable, despite being resolved at the retina. We here compare susceptibilities to auditory informational masking and visual crowding in the same participants. Surprisingly, across participants, we find a negative correlation (R = -0.7) between susceptibility to informational masking and crowding: Participants who have low susceptibility to auditory clutter tend to have high susceptibility to visual clutter, and vice versa. This reveals a tradeoff in the brain between auditory and visual processing.

Veterans with dizziness recruit compensatory saccades in each semicircular canal plane although VOR gain is normal.

BACKGROUND: Exposure to brain injury via blast or blunt mechanisms disrupts multiple sensorimotor systems simultaneously. Large numbers of US Gulf War era and Operation Iraqi/Enduring Freedom veterans with traumatic brain injury (TBI) are suffering the symptom of dizziness - presumed due to "Multi-Sensory Impairment", a clinical pattern of damage to the auditory, visual and vestibular sensorimotor systems. OBJECTIVE: To describe the oculomotor response to rapid head rotation in a population of veterans with dizziness. We also describe the reliability of using the video head impulse test (vHIT) in a veteran population. METHODS: We used the vHIT to evaluate the vestibular-ocular reflex (VOR) gain and presence of compensatory saccades (CS) in each semicircular canal of 81 veterans (31% TBI) with dizziness. Data was collected using the ICS Otometric™ vHIT. Data was processed using both the Otometric™ software and custom software written in MATLAB™. This data was evaluated through Kruskal-Wallis rank-sum test and analysis of regression. RESULTS: Veterans with dizziness recruit CS in all semicircular canal planes even though their VOR gain is normal. The vHIT is a reliable clinical test to quantify the metrics of the VOR and CS in veterans. CONCLUSION: Veterans with dizziness symptoms use compensatory saccades in all planes of semicircular canal rotation, despite having normal peripheral VOR gain during rapid head rotation. The video head impulse test is a stable measure of vestibular slow phase and metrics of compensatory saccades in veterans with dizziness.

NOSH-aspirin (NBS-1120) inhibits pancreatic cancer cell growth in a xenograft mouse model: Modulation of FoxM1, p53, NF-κB, iNOS, caspase-3 and ROS.

Pancreatic cancer has poor survival rates and largely ineffective therapies. Aspirin is the prototypical anti-cancer agent but its long-term use is associated with significant side effects. NOSH-aspirin belongs to a new class of anti-inflammatory agents that were designed to be safer alternatives by releasing nitric oxide and hydrogen sulfide. In this study we evaluated the effects of NOSH-aspirin against pancreatic cancer using cell lines and a xenograft mouse model. NOSH-aspirin inhibited growth of MIA PaCa-2 and BxPC-3 pancreatic cancer cells with IC50s of 47 ± 5, and 57 ± 4 nM, respectively, while it did not inhibit growth of a normal pancreatic epithelial cell line at these concentrations. NOSH-aspirin inhibited cell proliferation, caused G0/G1 phase cycle arrest, leading to increased apoptosis. Treated cells displayed increases in reactive oxygen species (ROS) and caspase-3 activity. In MIA PaCa-2 cell xenografts, NOSH-aspirin significantly reduced tumor growth and tumor mass. Growth inhibition was due to reduced proliferation (decreased PCNA expression) and induction of apoptosis (increased TUNEL positive cells). Expressions of ROS, iNOS, and mutated p53 were increased; while that of NF-κB and FoxM1 that were high in vehicle-treated xenografts were significantly inhibited by NOSH-aspirin. Taken together, these molecular events and signaling pathways contribute to NOSH-aspirin mediated growth inhibition and apoptotic death of pancreatic cancer cells in vitro and in vivo.