Can image-based virtual reality help teach anatomy?

OBJECTIVE: To assess the utilization of a novel virtual reality robotic surgical simulator (RoSS) in surgical anatomy training and pattern recognition. STUDY DESIGN: Ten surgical trainees (medical students and residents) were recruited to participate in a study that evaluated the efficacy of a robotic simulator in anatomy training. The subjects were divided into two groups of five individuals each. Each participant received a syllabus consisting of line diagrams and color pictures of the human anatomy. All participants were later tested on identifying the same five anatomical landmarks from photographs from actual laparoscopic procedures. Group I studied the syllabus and took the test. Group II similarly studied the syllabus, but were trained on the RoSS system using cognitive skill sets and then took the same test. Group II were asked to complete a posttest survey. RESULTS: Mean time to complete the test was 142.8 seconds for group I and 118.4 seconds for group II. Mean number of errors committed by the group trained on RoSS was 0.4 out of 5, whereas the group that did not undergo training on RoSS committed 1.7 out of 5. The mean number of correct answers given by group I was 2.9 out of 5, whereas group II answered 4.2 out 5 correctly. All results were statistically significant. The subjects rated the anatomy module helpful, with a mean rating of 3.6 out of 5. CONCLUSIONS: RoSS is an effective tool in anatomy training. Further testing is underway to illustrate its important role in medical education and robotic surgical training.

Methamphetamine alters blood brain barrier permeability via the modulation of tight junction expression: Implication for HIV-1 neuropathogenesis in the context of drug abuse.

The pathogenesis of human immunodeficiency virus (HIV) associated encephalopathy is attributed to infiltration of the central nervous system (CNS) by HIV-1 infected mononuclear cells that transmigrate across the blood brain barrier (BBB). The endothelial tight junctions (TJ) of the blood brain barrier (BBB) play a critical role in controlling cellular traffic into the CNS. Neuropathogenesis of HIV-1 is exacerbated by drugs of abuse such as methamphetamine (Meth) which are capable of dysregulating BBB function. HIV-1 viral proteins like gp120 are both neurotoxic and cytotoxic and have been implicated in the development of HIV-1 dementia (HAD). We hypothesize that gp120 in synergy with Meth can alter BBB permeability via the modulation of tight junction expression. We investigated the effect of Meth and/or gp120 on the basal expression of TJ proteins ZO-1, JAM-2, Occludin, Claudin-3 and Claudin-5, using in vitro cultures of the primary brain microvascular endothelial cells (BMVEC). Further, the functional effects of TJ modulation were assessed using an in vitro BBB model, that allowed measurement of BBB permeability using TEER measurements and transendothelial migration of immunocompetent cells. Our results show that both Meth and gp120 individually and in combination, modulated TJ expression, and these effects involved Rho-A activation. Further, both Meth and gp120 alone and in combination significantly decreased transendothelial resistance across the in vitro BBB and the enhanced transendothelial migration of immunocompetent cells across the BBB. An understanding of the mechanisms of BBB breakdown that lead to neurotoxicity is crucial to the development of therapeutic modalities for Meth abusing HAD patients.

Photopheresis in HIV-1 infected patients utilizing benzoporphyrin derivative (BPD) verteporfin and light.

An ex vivo trial utilizing photopheresis with Benzoporphyrin Derivative as the photoactive compound, identified the minimum energy levels of light and concentrations of BPD that eradicated both cell-free and cell-associated HIV-1 infectivity without destroying the virus particles or infected leukocytes. Leukocytes remained viable with altered chemokine/cytokine expression. Apoptosis was induced in a minority of CD4 but not CD8 positive cells with a statistically significant increase in cytolytic T-cell activity. In the 24 week clinical trial in 7 HIV-1 infected patients, three who had rapidly rising viral loads prior to initiating therapy stabilized. Two had a sustained greater than 0.5 log decrement and 5 had stable plasma viral loads (less than a 0.5 log increment or decrement) with varied effects on absolute CD4 and CD8 positive lymphocytes counts. One achieved a greater than 1 log decrement in HIV-1 plasma viral load and undetectable in vivo cell-free and cell-associated HIV-1 infectivity with an increased in vitro lymphocyte mitogen stimulation index. Under amended protocol, 5 additional 12 month courses were administered to three additional patients and two of the previous enrollees. Area under the curve for viral load showed a significant decrease from pre- to post-therapy (p 0.007). No associated toxicities were observed.