Can new passenger cars reduce pedestrian lower extremity injury? A review of geometrical changes of front-end design before and after regulatory efforts

<p><b>Objective</b>: Pedestrian lower extremity represents the most frequently injured body region in car-to-pedestrian accidents. The European Directive concerning pedestrian safety was established in 2003 for evaluating pedestrian protection performance of car models. However, design changes have not been quantified since then. The goal of this study was to investigate front-end profiles of representative passenger car models and the potential influence on pedestrian lower extremity injury risk.</p> <p><b>Methods</b>: The front-end styling of sedans and sport utility vehicles (SUV) released from 2008 to 2011 was characterized by the geometrical parameters related to pedestrian safety and compared to representative car models before 2003. The influence of geometrical design change on the resultant risk of injury to pedestrian lower extremity—that is, knee ligament rupture and long bone fracture—was estimated by a previously developed assessment tool assuming identical structural stiffness. Based on response surface generated from simulation results of a human body model (HBM), the tool provided kinematic and kinetic responses of pedestrian lower extremity resulted from a given car's front-end design.</p> <p><b>Results</b>: Newer passenger cars exhibited a “flatter” front-end design. The median value of the sedan models provided 87.5 mm less bottom depth, and the SUV models exhibited 94.7 mm less bottom depth. In the lateral impact configuration similar to that in the regulatory test methods, these geometrical changes tend to reduce the injury risk of human knee ligament rupture by 36.6 and 39.6% based on computational approximation. The geometrical changes did not significantly influence the long bone fracture risk.</p> <p><b>Conclusions</b>: The present study reviewed the geometrical changes in car front-ends along with regulatory concerns regarding pedestrian safety. A preliminary quantitative benefit of the lower extremity injury reduction was estimated based on these geometrical features. Further investigation is recommended on the structural changes and inclusion of more accident scenarios.</p

An energy-absorbing sliding seat for reducing neck injury risks in rear impact—analysis for prototype built

<p><b>Objective</b>: This study investigated overall performance of an energy-absorbing sliding seat concept for whiplash neck injury prevention. The sliding seat allows its seat pan to slide backward for some distance under certain restraint force to absorb crash energy in rear impacts.</p> <p><b>Methods</b>: A numerical model that consisted of vehicle interior, seat, seat belt, and BioRID II dummy was built in MADYMO to evaluate whiplash neck injury in rear impact. A parametric study of the effects of sliding seat parameters, including position and cushion stiffness of head restraint, seatback cushion stiffness, recliner characteristics, and especially sliding energy-absorbing (EA) restraint force, on neck injury criteria was conducted in order to compare the effectiveness of the sliding seat concept with that of other existing anti-whiplash mechanisms. Optimal sliding seat design configurations in rear crashes of different severities were obtained. A sliding seat prototype with bending of a steel strip as an EA mechanism was fabricated and tested in a sled test environment to validate the concept. The performance of the sliding seat under frontal and rollover impacts was checked to make sure the sliding mechanism did not result in any negative effects.</p> <p><b>Results</b>: The protective effect of the sliding seat with EA restraint force is comparable to that of head restraint–based and recliner stiffness–based anti-whiplash mechanisms. EA restraint force levels of 3 kN in rear impacts of low and medium severities and 6 kN in impacts of high severity were obtained from optimization. In frontal collision and rollover, compared to the nonsliding seat, the sliding seat does not result in any negative effects on occupant protection. The sled test results of the sliding seat prototype have shown the effectiveness of the concept for reducing neck injury risks.</p> <p><b>Conclusion</b>: As a countermeasure, the sliding seat with appropriate restraint forces can significantly reduce whiplash neck injury risk in rear impacts of low, medium, and high severities with no negative effects on other crash load cases.</p

In Situ Generation of Palladium Nanoparticles: Ligand-Free Palladium Catalyzed Pivalic Acid Assisted Carbonylative Suzuki Reactions at Ambient Conditions

Highly selective carbonylative Suzuki reactions of aryl iodides with arylboronic acids using an in situ generated nanopalladium system furnished products in high yields. The reactions were performed under ambient conditions and in the absence of an added ligand. The key to success is the addition of pivalic acid, which can effectively suppress undesired Suzuki coupling. The synthesis can be easily scaled up, and the catalytic system can be reused up to nine times. The nature of the active catalytic species are discussed

Immunofluorescence detection of tight junction correlated protein occludin in A549 cells.

<p>(A) DMSO control. (B) melatonin (0.1 mmol/L). (C) melatonin (2.0 mmol/L).</p

The effect of melatonin, SP600125 and PMA on migration of A549 cells.

<p>(A) The effect of melatonin, SP600125 and PMA on migration of A549 cells after 0 h, 12 h and 24 h. (B) Analysis of migration rate, compared with control group: *P<0.05, ^#P<0.05; compared with PMA group: ^▴P<0.05, ^△P<0.05.</p

The effect of different concentrations of MLT on the viability of A549 cells in 3 day.

<p>Compared with DMSO control group, *P<0.05.</p

The Effect of melatonin, SP600125 and PMA on the expression of occludin, OPN, MLCK and phosphorylation of MLC, JNK.

<p>(A) occludin, (B) OPN, (C) MLC and MLCK, (D) JNK. Results are presented as mean ± SD of three independent experiments. *<i>P</i><0.05,^#P<0.05, in comparison to control; ^▴P<0.05, ^△P<0.05, in comparison to PMA group.</p

Effects of lanthanum and acid rain stress on the bio-sequestration of lanthanum in phytoliths in germinated rice seeds

<div><p>REEs in the environment can be absorbed by plants and sequestered by plant phytoliths. Acid rain can directly or indirectly affect plant physiological functions. Currently, the effects of REEs and acid rain on phytolith-REEs complex in plants are not yet fully understood. In this study, a high-silicon accumulation crop, rice (<i>Oryza sativa</i> L.), was selected as a representative of plants, and orthogonal experiments were conducted under various levels of lanthanum [La(III)] and pH. The results showed that various La(III) concentrations could significantly improve the efficiency and sequestration of phytolith La(III) in germinated rice seeds. A pH of 4.5 promoted phytolith La(III) sequestration, while a pH of 3.5 inhibited sequestration. Compared with the single treatment with La(III), the combination of La(III) and acid rain inhibited the efficiency and sequestration of phytolith La(III). Correlation analysis showed that the efficiency of phytolith La(III) sequestration had no correlation with the production of phytolith but was closely correlated with the sequestration of phytolith La(III) and the physiological changes of germinated rice seeds. Phytolith morphology was an important factor affecting phytolith La(III) sequestration in germinated rice seeds, and the effect of tubes on sequestration was more significant than that of dumbbells. This study demonstrated that the formation of the phytolith and La(III) complex could be affected by exogenous La(III) and acid rain in germinated rice seeds.</p></div

A Kir6.2 Pore Mutation Causes Inactivation of ATP-Sensitive Potassium Channels by Disrupting PIP₂-Dependent Gating

<div><p>In the absence of intracellular nucleotides, ATP-sensitive potassium (K_ATP) channels exhibit spontaneous activity via a phosphatidylinositol-4,5-bisphosphate (PIP₂)-dependent gating process. Previous studies show that stability of this activity requires subunit-subunit interactions in the cytoplasmic domain of Kir6.2; selective mutagenesis and disease mutations at the subunit interface result in time-dependent channel inactivation. Here, we report that mutation of the central glycine in the pore-lining second transmembrane segment (TM2) to proline in Kir6.2 causes K_ATP channel inactivation. Unlike C-type inactivation, a consequence of selectivity filter closure, in many K⁺ channels, the rate of inactivation in G156P channels was insensitive to changes in extracellular ion concentrations or ion species fluxing through the pore. Instead, the rate of G156P inactivation decreased with exogenous application of PIP₂ and increased when PIP₂-channel interaction was inhibited with neomycin or poly-L-lysine. These findings indicate the G156P mutation reduces the ability of PIP₂ to stabilize the open state of K_ATP channels, similar to mutations in the cytoplasmic domain that produce inactivation. Consistent with this notion, when PIP₂-dependent open state stability was substantially increased by addition of a second gain-of-function mutation, G156P inactivation was abolished. Importantly, bath application and removal of Mg²⁺-free ATP or a nonhydrolyzable analog of ATP, which binds to the cytoplasmic domain of Kir6.2 and causes channel closure, recover G156P channel from inactivation, indicating crosstalk between cytoplasmic and transmembrane domains. The G156P mutation provides mechanistic insight into the structural and functional interactions between the pore and cytoplasmic domains of Kir6.2 during gating.</p></div

WDR1 forms a complex with TbCUL4 and TbDDB1.

<p>(<b>A</b>). Alignment of the putative DWD box in WDR1 with the DWD box of fission yeast and human WD40-repeat proteins that have been confirmed to bind to DDB1. The three highly conserved residues are highlighted in red, and other conserved residues are in green. The consensus sequence of the DWD box is shown at the top of the aligned sequences. Tb, <i>T</i>. <i>brucei</i>; Sp, <i>Schizosaccharomyces pombe</i>; Hs, <i>Homo sapiens</i>. (<b>B</b>). WDR1 interacts with TbCUL4 but not other Cullin proteins, in <i>T</i>. <i>brucei</i>, as demonstrated by co-immunoprecipitation. WDR1-3HA and each of the five PTP-tagged Cullin proteins were co-expressed from their respective endogenous locus in <i>T</i>. <i>brucei</i>. Immunoprecipitation was performed by incubating the cell lysate with IgG beads, and immunoprecipitated proteins were then immunoblotted with anti-HA antibody and anti-Protein A (α-ProtA) antibody, respectively. (<b>C</b>). WDR1 interacts with TbDDB1 <i>in vivo</i> in <i>T</i>. <i>brucei</i>, as demonstrated by co-immunoprecipitation. WDR1-3HA and TbDDB1-PTP were co-expressed in <i>T</i>. <i>brucei</i>, and immunoprecipitation and Western blotting were performed as described in panel B. (<b>D</b>). WDR1, TbCUL4, TbDDB1 and TbPLK form a complex in <i>T</i>. <i>brucei</i>, as demonstrated by co-immunoprecipitation. WDR1-3HA, TbCUL4-PTP and TbDDB1-3Myc were co-expressed from their respective endogenous locus in <i>T</i>. <i>brucei</i>. Immunoprecipitation of WDR1-3HA was carried out by incubating the cell lysate with EZview Red anti-HA affinity gel, and immunoprecipitated proteins were immunoblotted with anti-HA antibody, anti-Myc antibody, anti-TbPLK antibody and anti-Protein A (α-ProtA) antibody to detect WDR1-3HA, TbDDB1-3Myc, TbPLK and TbCUL4-PTP, respectively. (<b>E</b>). The N-terminal domain of WDR1 mediates the interaction with TbDDB1, as demonstrated by <i>in vitro</i> GST pull-down. The N-terminal fragment (1–300 aa) of WDR1, which contains the WD40 motif, was expressed as a GST-fusion protein in <i>E</i>. <i>coli</i>, purified and used to pull down TbDDB1-3HA from <i>T</i>. <i>brucei</i> cell lysate. Purified GST-WDR1^1-300 and GST were stained by coomassie brilliant blue (CBB).</p