Multi-modal virtual scenario enhances neurofeedback learning

In the past decade neurofeedback (NF) has become the focus of a growing body of research. With real-time functional magnetic resonance imaging (fMRI) enabling online monitoring of emotion-related areas, such as the amygdala, many have begun testing its therapeutic benefits. However, most existing NF procedures still use monotonic uni-modal interfaces, thus possibly limiting user engagement and weakening learning efficiency. The current study tested a novel multi-sensory NF animated scenario (AS) aimed at enhancing user experience and improving learning. We examined whether relative to a simple uni-modal 2D interface, learning via an interface of complex multi-modal 3D scenario will result in improved NF learning. As a neural-probe, we used the recently developed fMRI-inspired EEG model of amygdala activity (“amygdala-EEG finger print”; amygdala-EFP), enabling low-cost and mobile limbic NF training. Amygdala-EFP was reflected in the AS by the unrest level of a hospital waiting room in which virtual characters become impatient, approach the admission desk and complain loudly. Successful downregulation was reflected as an ease in the room unrest level. We tested whether relative to a standard uni-modal 2D graphic thermometer (TM) interface, this AS could facilitate more effective learning and improve the training experience. Thirty participants underwent two separated NF sessions (1 week apart) practicing downregulation of the amygdala-EFP signal. In the first session, half trained via the AS and half via a TM interface. Learning efficiency was tested by three parameters: (a) effect size of the change in amygdala-EFP following training, (b) sustainability of the learned downregulation in the absence of online feedback, and (c) transferability to an unfamiliar context. Comparing amygdala-EFP signal amplitude between the last and the first NF trials revealed that the AS produced a higher effect size. In addition, NF via the AS showed better sustainability, as indicated by a no-feedback trial conducted in session 2 and better transferability to a new unfamiliar interface. Lastly, participants reported that the AS was more engaging and more motivating than the TM. Together, these results demonstrate the promising potential of integrating realistic virtual environments in NF to enhance learning and improve user’s experience

Release of Neutrophil Extracellular Traps by Neutrophils Stimulated With Antiphospholipid Antibodies: A Newly Identified Mechanism of Thrombosis in the Antiphospholipid Syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/115902/1/art39247.pd

Establishment of canine hemangiosarcoma xenograft models expressing endothelial growth factors, their receptors, and angiogenesis-associated homeobox genes

<p>Abstract</p> <p>Background</p> <p>Human hemangiosarcoma (HSA) tends to have a poor prognosis; its tumorigenesis has not been elucidated, as there is a dearth of HSA clinical specimens and no experimental model for HSA. However, the incidence of spontaneous HSA is relatively high in canines; therefore, canine HSA has been useful in the study of human HSA. Recently, the production of angiogenic growth factors and their receptors in human and canine HSA has been reported. Moreover, the growth-factor environment of HSA is very similar to that of pathophysiological angiogenesis, which some homeobox genes regulate in the transcription of angiogenic molecules. In the present study, we established 6 xenograft canine HSA tumors and detected the expression of growth factors, their receptors, and angiogenic homeobox genes.</p> <p>Methods</p> <p>Six primary canine HSAs were xenografted to nude mice subcutaneously and serially transplanted. Subsequently, the expressions of vascular endothelial growth factor (VEGF)-A, basic fibroblast growth factors (bFGF), flt-1 and flk-1 (receptors of VEGF-A), FGFR-1, and angiogenic homeobox genes HoxA9, HoxB3, HoxB7, HoxD3, Pbx1, and Meis1 were investigated in original and xenograft tumors by histopathology, immunostaining, and reverse transcription polymerase chain reaction (RT-PCR), using canine-specific primer sets.</p> <p>Results</p> <p>Histopathologically, xenograft tumors comprised a proliferation of neoplastic cells that were varied in shape, from spindle-shaped and polygonal to ovoid; some vascular-like structures and vascular clefts of channels were observed, similar to those in the original tumors. The expression of endothelial markers (CD31 and vWF) was detected in xenograft tumors by immunohistochemistry and RT-PCR. Moreover, the expression of VEGF-A, bFGF, flt-1, flk-1, FGFR-1, HoxA9, HoxB3, HoxB7, HoxD3, Pbx1, and Meis1 was detected in xenograft tumors. Interestingly, expressions of bFGF tended to be higher in 3 of the xenograft HSA tumors than in the other tumors.</p> <p>Conclusion</p> <p>We established 6 xenograft canine HSA tumors in nude mice and found that the expressions of angiogenic growth factors and their receptors in xenograft HSAs were similar to those in spontaneous HSA. Furthermore, we detected the expression of angiogenic homeobox genes; therefore, xenograft models may be useful in analyzing malignant growth in HSA.</p

Systems biology of platelet-vessel wall interactions

Platelets are small, anucleated cells that participate in primary hemostasis by forming a hemostatic plug at the site of a blood vessel's breach, preventing blood loss. However, hemostatic events can lead to excessive thrombosis, resulting in life-threatening strokes, emboli, or infarction. Development of multi-scale models coupling processes at several scales and running predictive model simulations on powerful computer clusters can help interdisciplinary groups of researchers to suggest and test new patient-specific treatment strategies

New insights into the mechanisms of venous thrombosis

Venous thrombosis is a leading cause of morbidity and mortality in industrialized countries, especially in the elderly. Many risk factors have been identified for venous thrombosis that alter blood flow, activate the endothelium, and increase blood coagulation. However, the precise mechanisms that trigger clotting in large veins have not been fully elucidated. The most common site for initiation of the thrombus appears to be the valve pocket sinus, due to its tendency to become hypoxic. Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis. Understanding the mechanisms of venous thrombosis may lead to the development of new treatments