ASSESSMENT OF TRAVEL SPEED FOR URBAN STREETS USING GLOBAL POSITIONING SYSTEM

The travel speeds selected and trusted by the driver vary according to his behavior and the surrounding environment. Accordingly, this paper studies the change of the free-flow speed, influences on it, of the route linking Al-Bayaa and Bab Almudam sectors. A GPS device was used to collect data during 60 rounds for three periods (morning, day, and night), 50 of them during the off-peak time and 10 during peak time with drivers of both genders and different ages. The results showed a variation of the FFS values at off-evening peak time, also noting the posted speed limits corresponding to the statistically calculated 85, which was 69km\hr. along the route. The emergence of a significant impact of the security checkpoints in link 3, causing a general defect in the traffic accounts. Also, there was an increase in the speed with an increase in lane width by 13% and a decrease in the speed with an increase in the number of lanes by 45.18% and 18.6% between 2 and 4 lanes and 2 and 3 lanes respectively. It should be noted that male is bolder and more reckless in choosing speeds by 26.32% than female and that groups of 50 and below years old choose less speed by 13.52% of ages 35 and below years old who are more confident and familiar in dealing with roads and choosing the appropriate speed.

Elevating PI3P drives select downstream membrane trafficking pathways

Phosphoinositide signaling lipids are essential for several cellular processes. The requirement for a phosphoinositide is conventionally studied by depleting the corresponding lipid kinase. However, there are very few reports on the impact of elevating phosphoinositides. That phosphoinositides are dynamically elevated in response to stimuli suggests that, in addition to being required, phosphoinositides drive downstream pathways. To test this hypothesis, we elevated the levels of phosphatidylinositol-3-phosphate (PI3P) by generating hyperactive alleles of the yeast phosphatidylinositol 3-kinase, Vps34. We find that hyperactive Vps34 drives certain pathways, including PI(3,5)P2 synthesis and retrograde transport from the vacuole. This demonstrates that PI3P is rate limiting in some pathways. Interestingly, hyperactive Vps34 does not affect ESCRT function. Thus, elevating PI3P does not always increase the rate of PI3P-dependent pathways. Elevating PI3P can also delay a pathway. Elevating PI3P slowed late steps in autophagy, in part by delaying the disassembly of autophagy proteins from mature autophagosomes as well as delaying fusion of autophagosomes with the vacuole. This latter defect is likely due to a more general defect in vacuole fusion, as assessed by changes in vacuole morphology. These studies suggest that stimulus-induced elevation of phosphoinositides provides a way for these stimuli to selectively regulate downstream processes.

The Devil is in the Defects: Electronic Conductivity in Solid Electrolytes

Rechargeable solid-state batteries continue to gain prominence due to their increased safety. However, a number of outstanding challenges have prevented their adoption in mainstream technology. In this study, we reveal the origins of electronic conductivity (s_e) in solid electrolytes (SEs), which is deemed responsible for solid-state battery degradation, as well as more drastic short-circuit and failure. Using first-principles defect calculations and physics-based models, we predict s_e in three topical SEs: Li₆PS₅Cl and Li₆PS₅I argyrodites, and Na₃PS₄ for post-Li batteries. We treat SEs as materials with finite band gaps and apply the defect theory of semiconductors to calculate the native defect concentrations and associated electronic conductivities. Our experimental measurements of the band gap of tetragonal Na₃PS₄ confirm our predictions. The quantitative agreement of the predicted s_e in these three materials and those measured experimentally strongly suggests that self-doping via native defects is the primary source of electronic conductivity in SEs. In particular, we find that Li₆PS₅X are <i>n</i>-type (electrons are majority carriers), while Na₃PS₄ is <i>p</i>-type (holes). Importantly, the predicted values set the lower bound for s_e in SEs. We suggest general defect engineering strategies pertaining to synthesis protocols to reduce s_e in SEs, and thereby, curtailing the degradation of solid-state batteries. The methodology presented here can be extended to investigate s_e in secondary phases that typically form at electrode-electrolyte interfaces, as well as to complex oxide-based SEs.

The Devil is in the Defects: Electronic Conductivity in Solid Electrolytes

Rechargeable solid-state batteries continue to gain prominence due to their increased safety. However, a number of outstanding challenges have prevented their adoption in mainstream technology. In this study, we reveal the origins of electronic conductivity (s_e) in solid electrolytes (SEs), which is deemed responsible for solid-state battery degradation, as well as more drastic short-circuit and failure. Using first-principles defect calculations and physics-based models, we predict s_e in three topical SEs: Li₆PS₅Cl and Li₆PS₅I argyrodites, and Na₃PS₄ for post-Li batteries. We treat SEs as materials with finite band gaps and apply the defect theory of semiconductors to calculate the native defect concentrations and associated electronic conductivities. Our experimental measurements of the band gap of tetragonal Na₃PS₄ confirm our predictions. The quantitative agreement of the predicted s_e in these three materials and those measured experimentally strongly suggests that self-doping via native defects is the primary source of electronic conductivity in SEs. In particular, we find that Li₆PS₅X are <i>n</i>-type (electrons are majority carriers), while Na₃PS₄ is <i>p</i>-type (holes). Importantly, the predicted values set the lower bound for s_e in SEs. We suggest general defect engineering strategies pertaining to synthesis protocols to reduce s_e in SEs, and thereby, curtailing the degradation of solid-state batteries. The methodology presented here can be extended to investigate s_e in secondary phases that typically form at electrode-electrolyte interfaces, as well as to complex oxide-based SEs.

2D Material Science: Defect Engineering by Particle Irradiation

Two-dimensional (2D) materials are at the heart of many novel devices due to their unique and often superior properties. For simplicity, 2D materials are often assumed to exist in their text-book form, i.e., as an ideal solid with no imperfections. However, defects are ubiquitous in macroscopic samples and play an important – if not imperative – role for the performance of any device. Thus, many independent studies have targeted the artificial introduction of defects into 2D materials by particle irradiation. In our view it would be beneficial to develop general defect engineering strategies for 2D materials based on a thorough understanding of the defect creation mechanisms, which may significantly vary from the ones relevant for 3D materials. This paper reviews the state-of-the-art in defect engineering of 2D materials by electron and ion irradiation with a clear focus on defect creation on the atomic scale and by individual impacts. Whenever possible we compile reported experimental data alongside corresponding theoretical studies. We show that, on the one hand, defect engineering by particle irradiation covers a wide range of defect types that can be fabricated with great precision in the most commonly investigated 2D materials. On the other hand, gaining a complete understanding still remains a challenge, that can be met by combining advanced theoretical methods and improved experimental set-ups, both of which only now begin to emerge. In conjunction with novel 2D materials, this challenge promises attractive future opportunities for researchers in this field.

Lack of functional caveolae in Cav3 mutated human dystrophic myotubes results in deficient mechanoprotection and IL6/STAT3 mechanosignaling

Caveolin-3 is the major structural protein of caveolae in muscle cells. Mutations in the CAV3 gene cause different type of muscle disorders mostly characterized by defects in membrane integrity and repair, deregulation in the expression of various muscle proteins and deregulation of several muscle associated signaling pathways. We show here that myotubes derived from patients bearing the CAV3 P28L and R26Q mutations present a lack of functional caveolae at the plasma membrane which results in an abnormal mechanoresponse. Mutant myotubes can no longer buffer the increase of membrane tension induced by mechanical stress and present an hyperactivation of the IL6/STAT3 signaling pathway at rest and under mechanical stress. The impaired mechanical regulation of the IL6/STAT3 signaling pathway by caveolae leads to chronic activation and a higher expression of muscle specific genes. These defects could be reversed by reassembling a pool of functional caveolae through expression of wild type Cav3. Our findings bring more mechanistic insight into human Cav3 associated muscle disorders and show a general defect in the mechanoresponse of CAV3 P28L and R26Q myotubes.

Defects on carbons for electrocatalytic oxygen reduction

A general defect promoted catalysis mechanism is established to reveal the active sites of various defective carbon based ORR electrocatalysts.

Relating defect chemistry and electronic transport in the double perovskite Ba1−xGd0.8La0.2+xCo2O6−δ (BGLC)

A general defect chemical model is applied to the double perovskite BGLC and used rationalize its physiochemical and electrical properties.

A Novel Scan-Based Yield Enhancement Methodology for Faster Yield Ramp

Scan chain integrity yield loss is a common concern, especially in early stage of product yield ramp. Typically, scan chain failure diagnosis can only proceed upon full silicon build and structural test. In this work, we propose a proactive methodology which enables failure debug step to be initiated as early as the onset of device fabrication, to bring forward yield learning. Scan chain cells and nets information are extracted from design data file and converted to inline optical wafer inspection care areas. In this way, the inspection recipe can be optimized for the detection of scan chain related defects. It is shown experimentally that such approach can potentially enhance general defect detection sensitivity by 50% and increase the defect hit probability on scan chain nets. Any findings serve as useful early data for process improvement feedback. Furthermore, marginal defects, which otherwise are not easily revealed using conventional approach, can also be detected to provide early warning for process drifts or variations.