On the Design of a Dual-Mode User Interface for Accessing 3D Content on the World Wide Web

International audienceThe World Wide Web, today's largest and most important online information infrastructure, does not support 3D content and, although various approaches have been proposed, there is still no clear design methodology for user interfaces that tightly integrate hypertext and interactive 3D graphics. This paper presents a novel strategy for accessing information spaces, where hypertext and 3D graphics data are simultaneously available and interlinked. We introduce a Dual-Mode User Interface that has two modes between which a user can switch anytime: the driven by simple hypertext-based interactions "hypertext mode", where a 3D scene is embedded in hypertext and the more immersive "3D mode", which immerses the hypertextual annotations into the 3D scene. A user study is presented, which characterizes the interface in terms of its efficiency and usability

Insulin increases glomerular filtration barrier permeability through PKGIα-dependent mobilization of BKCa channels in cultured rat podocytes

AbstractPodocytes are highly specialized cells that wrap around glomerular capillaries and comprise a key component of the glomerular filtration barrier. They are uniquely sensitive to insulin; like skeletal muscle and fat cells, they exhibit insulin-stimulated glucose uptake and express glucose transporters. Podocyte insulin signaling is mediated by protein kinase G type I (PKGI), and it leads to changes in glomerular permeability to albumin. Here, we investigated whether large-conductance Ca2+-activated K+ channels (BKCa) were involved in insulin-mediated, PKGIα-dependent filtration barrier permeability.Insulin-induced glomerular permeability was measured in glomeruli isolated from Wistar rats. Transepithelial albumin flux was measured in cultured rat podocyte monolayers. Expression of BKCa subunits was detected by RT-PCR. BKCa, PKGIα, and upstream protein expression were examined in podocytes with Western blotting and immunofluorescence. The BKCa–PKGIα interaction was assessed with co-immunoprecipitation.RT-PCR showed that primary cultured rat podocytes expressed mRNAs that encoded the pore-forming α subunit and four accessory β subunits of BKCa. The BKCa inhibitor, iberiotoxin (ibTX), abolished insulin-dependent glomerular albumin permeability and PKGI-dependent transepithelial albumin flux. Insulin-evoked albumin permeability across podocyte monolayers was also blocked with BKCa siRNA. Moreover, ibTX blocked insulin-induced disruption of the actin cytoskeleton and changes in the phosphorylation of PKG target proteins, MYPT1 and RhoA.These results indicated that insulin increased filtration barrier permeability through mobilization of BKCa channels via PKGI in cultured rat podocytes. This molecular mechanism may explain podocyte injury and proteinuria in diabetes

Metformin reduces NAD(P)H oxidase activity in mouse cultured podocytes through purinergic dependent mechanism by increasing extracellular ATP concentration

Hyperglycemia affects the functioning numbers of podocytes and leads to a gradual decline of renal function. The normalization of glucose level is a principle therapeutic goal in diabetic patients and metformin is a popular hypoglycemic drug used in type 2 diabetes mellitus. Metformin activates AMP-activated kinase (AMPK) and decreases NAD(P)H oxidase activity in podocytes leading to reduction of free radical generation. Similar effects are observed after activation of P2 receptors. Therefore, we investigated whether metformin increases extracellular ATP concentration and affects the activities of NAD(P) H oxidase and AMPK through P2 receptors. Experiments were performed on cultured mouse podocytes. NAD(P) H oxidase activity was measured by chemiluminescence and changes in AMPK activity were estimated by immunoblotting against AMPKα-Thr 172 -P. Metformin increased extracellular ATP concentration by reduction of ectoATPase activity, decreased NAD(P)H oxidase activity and increased AMPK phosphorylation. A P2 receptor antagonist, suramin (300 µM), prevented metformin action on NAD(P)H oxidase and AMPK phosphorylation. The data suggests a novel mechanism of metformin action, at least in podocytes. Metformin, which increases extracellular ATP concentration leads to activation of P2 receptors and consequent modulation of the podocytes' metabolism through AMPK and NAD(P)H oxidase which, in turn, may affect podocyte functioning

Research on the methods for calculating the width of the approach channel to the port

An approach channel to the port is a very important part of port infrastructure ensuring navigational safety of the ships entering and departing the port. Various methods used for determining the width of the approach channel to the port provide different results. Sometimes, variations are significant and make difficulties in arriving at the correct final decision. The article analyses diverse methods for research on calculating the width of the approach channel to the port. The obtained results have been verified conducting a real experiment involving real ships passing under similar hydro-meteorological conditions. The evaluation of the results and recommendations presented in the article can be used for the optimization and design of approach channels to ports

Detection of a glitch in the pulsar J1709-4429

We report the detection of a glitch event in the pulsar J1709$-$4429 (also known as B1706$-$44) during regular monitoring observations with the Molonglo Observatory Synthesis Telescope (UTMOST). The glitch was found during timing operations, in which we regularly observe over 400 pulsars with up to daily cadence, while commensally searching for Rotating Radio Transients, pulsars, and FRBs. With a fractional size of $\Delta\nu/\nu \approx 52.4 \times10^{-9}$, the glitch reported here is by far the smallest known for this pulsar, attesting to the efficacy of glitch searches with high cadence using UTMOST.Comment: 3 pages, 1 figur

Fracture risk in obesity: a narrative review

While low body mass index (BMI) is a risk factor for fractures, the association between obesity and fracture risk is inconsistent and puzzling. Several studies reported higher fracture risk (FR), and others reported lower FR in obese populations. Our narrative review presents the overall incidence of fractures by anatomic locations in adult patients, geriatric populations, and in those after bariatric surgery. In conclusion, obesity should be considered as a fracture risk in adults, as well as falls and fractures in geriatric patients, in particular in those with sarcopenic obesity, and after bariatric surgery. The specific characteristics of fractures risk associated with obesity should be considered by physicians in the diagnostic and therapeutic work-up of obese patients. This review outlines the current literature on this topic and aims to guide physicians regarding proper decisions to prevent fractures in patients with obesity