Effect of pedestrian physique differences on head injury prediction in car-to-pedestrian accidents using deep learning.

Objective: The aim of this study is to identify the effects of pedestrian physique differences on head injury prediction in car-to-pedestrian accidents via deep learning.

Methods: A series of parametric studies was carried out using a family car finite element model and MADYMO pedestrian models (AM50, AF05, 6YO). The car model was developed and tuned by 11 impact tests.

Application of Deep Learning Methods for Pedestrian Collision Detection Using Dashcam Videos.

The goal of this study is to clarify the usefulness of deep learning methods for pedestrian collision detection using dashcam videos for advanced automatic collision notification, focusing on pedestrians, as they make up the highest number of traffic fatalities in Japan. First, we created a dataset for deep learning from dashcam videos. A total of 78 dashcam videos of pedestrian-to-automobile accidents were collected from a video hosting website and from the Japan Automobile Research Institute (JARI).

Efficacy of FGF-2 in Periodontal Regeneration in a Case of Severe Intrabony Defect and Furcation Involvement With 15-Month Follow-Up.

Introduction: Several studies have demonstrated that basic fibroblast growth factor (FGF-2) is one of the most effective growth factors for periodontal regeneration. The Ministry of Health, Labor and Welfare in Japan have approved 0.3% human recombinant FGF-2 for periodontal regeneration, and it has been commercially available since 2016.

ZFAND5/ZNF216 is an activator of the 26S proteasome that stimulates overall protein degradation.

ZFAND5/ZNF216, a member of the zinc finger AN1-type domain family, is abundant in heart and brain, but is induced in skeletal muscle during atrophy (although not in proteotoxic stress). Because mice lacking ZFAND5 exhibit decreased atrophy, a role in stimulating protein breakdown seemed likely. Addition of recombinant ZFAND5 to purified 26S proteasomes stimulated hydrolysis of ubiquitinated proteins, short peptides, and ATP.

A Ferric-Peroxo Intermediate in the Oxidation of Heme by IsdI.

The canonical heme oxygenases (HOs) catalyze heme oxidation via a heme-bound hydroperoxo intermediate that is stabilized by a water cluster at the active site of the enzyme. In contrast, the hydrophobic active site of IsdI, a heme-degrading enzyme from Staphylococcus aureus, lacks a water cluster and is expected to oxidize heme by an alternative mechanism. Reaction of the IsdI-heme complex with either H2O2 or m-chloroperoxybenzoic acid fails to produce a specific oxidized heme iron intermediate, suggesting that ferric-hydroperoxo or ferryl derivatives of IsdI are not involved in the catalytic mechanism of this enzyme.

Effect of rebamipide on gastric bleeding and ulcerogenic responses induced by aspirin plus clopidogrel under stimulation of acid secretion in rats.

Background And Aim: We examined the prophylactic effect of rebamipide on gastric bleeding induced by the perfusion of aspirin (acetylsalicylic acid [ASA]) plus clopidogrel under the stimulation of acid secretion in rats.

Methods: Under urethane anesthesia, acid secretion was stimulated by the i.v.

Hsp70-Bag3 interactions regulate cancer-related signaling networks.

Bag3, a nucleotide exchange factor of the heat shock protein Hsp70, has been implicated in cell signaling. Here, we report that Bag3 interacts with the SH3 domain of Src, thereby mediating the effects of Hsp70 on Src signaling. Using several complementary approaches, we established that the Hsp70-Bag3 module is a broad-acting regulator of cancer cell signaling by modulating the activity of the transcription factors NF-κB, FoxM1, Hif1α, the translation regulator HuR, and the cell-cycle regulators p21 and survivin.

Comparative effects of the anti-platelet drugs, clopidogrel, ticlopidine, and cilostazol on aspirin-induced gastric bleeding and damage in rats.

Aims: The present study compared the effects of frequently used anti-platelet drugs, such as clopidogrel, ticlopidine, and cilostazol, on the gastric bleeding and ulcerogenic responses induced by intraluminal perfusion with 25 mM aspirin acidified with 25 mM HCl (acidified ASA) in rats.

Main Methods: The stomach was perfused with acidified ASA at a rate of 0.4 ml/min for 60 min under urethane anesthesia, and gastric bleeding was measured as the concentration of hemoglobin in the luminal perfusate, which was collected every 15 min.

Synthesis of L-2,3-diaminopropionic acid, a siderophore and antibiotic precursor.

L-2,3-diaminopropionic acid (L-Dap) is an amino acid that is a precursor of antibiotics and staphyloferrin B a siderophore produced by Staphylococcus aureus. SbnA and SbnB are encoded by the staphyloferrin B biosynthetic gene cluster and are implicated in L-Dap biosynthesis. We demonstrate here that SbnA uses PLP and substrates O-phospho-L-serine and L-glutamate to produce a metabolite N-(1-amino-1-carboxyl-2-ethyl)-glutamic acid (ACEGA).

Animal models of gastric bleeding induced by dual antiplatelet therapy using aspirin and clopidogrel--prophylactic effect of antiulcer drugs.

We set up two models of gastric bleeding in rats using low-dose aspirin (ASA) and the antiplatelet drug clopidogrel, a P2Y₁₂ receptor antagonist, and examined the effect of antiulcer drugs on gastric bleeding and ulcerogenic responses under such conditions. Under urethane anesthesia, two catheters were inserted into the rat stomach, one from the esophagus and another through the pylorus via an incision in the duodenum. In the first model, the stomach was perfused with 25 mM ASA dissolved in 50 mM HCl using an infusion pump, and gastric bleeding was measured as the hemoglobin concentration in perfusate collected every 15 min.

Single molecule force spectroscopy reveals that iron is released from the active site of rubredoxin by a stochastic mechanism.

Metal centers in metalloproteins involve multiple metal-ligand bonds. The release of metal ions from metalloproteins can have significant biological consequences, so understanding of the mechanisms by which metal ion dissociates has broad implications. By definition, the release of metal ions from metalloproteins involves the disruption of multiple metal-ligand bonds, and this process is often accompanied by unfolding of the protein.

Cytochrome b5 from Giardia lamblia.

The protozoan intestinal parasite Giardia lamblia lacks mitochondria and the ability to make haem yet encodes several putative haem-binding proteins, including three of the cytochrome b(5) family. We cloned one of these (gCYTb5-I) and expressed it within Escherichia coli as a soluble holoprotein. UV-visible and resonance Raman spectra of gCYTb5-I resemble those of microsomal cytochrome b(5), and homology modelling supports a structure in which a pair of invariant histidine residues act as axial ligands to the haem iron.

Inactivation of the heme degrading enzyme IsdI by an active site substitution that diminishes heme ruffling.

IsdG and IsdI are paralogous heme degrading enzymes from the bacterium Staphylococcus aureus. Heme bound by these enzymes is extensively ruffled such that the meso-carbons at the sites of oxidation are distorted toward bound oxygen. In contrast, the canonical heme oxygenase family degrades heme that is bound with minimal distortion.

Kinematics of the unrestrained vehicle occupants in side-impact crashes.

A test series involving direct right-side impact of a moving wall on unsupported, unrestrained cadavers with no arms was undertaken to better understand human kinematics and injury mechanisms during side impact at realistic speeds. The tests conducted provided a unique opportunity for a detailed analysis of the kinematics resulting from side impact. Specifically, this study evaluated the 3-dimensional (3D) kinematics of 3 unrestrained male cadavers subjected to lateral impact by a multi-element load wall carried by a pneumatically propelled rail-mounted sled reproducing a conceptual side crash impact.

Hydrogen bond strength modulates the mechanical strength of ferric-thiolate bonds in rubredoxin.

It has long been recognized that hydrogen bonds formed by protein backbone amides with cysteinyl S(γ) atoms play important roles in modulating the functional and structural properties of the iron-sulfur centers in proteins. Here we use single molecule atomic force microscopy, cyclic voltammetry, and protein engineering techniques to investigate directly how the strength of N-H···S(γ) hydrogen bonds in the secondary coordination sphere affects the mechanical stability of Fe(III)-thiolate bonds of rubredoxin. Our results show that the mechanical stability of Fe(III)-thiolate bonds in rubredoxin correlates with the strength of N-H···S(γ) hydrogen bonds as reflected by the midpoint reduction potential, providing direct evidence that N-H···S(γ) hydrogen bonds play important roles in modulating the mechanical and kinetic properties of the Fe(III)-thiolate bonds of iron-sulfur proteins and corroborating the important roles of the protein environment in tuning the properties of metal-thiolate bonds.

Electronic properties of the highly ruffled heme bound to the heme degrading enzyme IsdI.

IsdI, a heme-degrading protein from Staphylococcus aureus, binds heme in a manner that distorts the normally planar heme prosthetic group to an extent greater than that observed so far for any other heme-binding protein. To understand better the relationship between this distinct structural characteristic and the functional properties of IsdI, spectroscopic, electrochemical, and crystallographic results are reported that provide evidence that this heme ruffling is essential to the catalytic activity of the protein and eliminates the need for the water cluster in the distal heme pocket that is essential for the activity of classical heme oxygenases. The lack of heme orientational disorder in (1)H-NMR spectra of the protein argues that the catalytic formation of β- and δ-biliverdin in nearly equal yield results from the ability of the protein to attack opposite sides of the heme ring rather than from binding of the heme substrate in two alternative orientations.

N-terminal short fragment of TUP1 confers resistance to 5-bromodeoxyuridine in the yeast Saccharomyces cerevisiae.

Small molecules that exhibit biological activity have contributed to the understanding of the molecular mechanisms of various biological phenomena. 5-Bromodeoxyuridine (BrdU) is a thymidine analogue that modulates various biological phenomena such as cellular differentiation and cellular senescence in cultured mammalian cells. Although BrdU is thought to function through changing chromatin structure and gene expression, its precise molecular mechanisms are not understood.

BAG3 directly interacts with mutated alphaB-crystallin to suppress its aggregation and toxicity.

A homozygous disruption or genetic mutation of the bag3 gene causes progressive myofibrillar myopathy in mouse and human skeletal and cardiac muscle disorder while mutations in the small heat shock protein αB-crystallin gene (CRYAB) are reported to be responsible for myofibrillar myopathy. Here, we demonstrate that BAG3 directly binds to wild-type αB-crystallin and the αB-crystallin mutant R120G, via the intermediate domain of BAG3. Peptides that inhibit this interaction in an in vitro binding assay indicate that two conserved Ile-Pro-Val regions of BAG3 are involved in the interaction with αB-crystallin, which is similar to results showing BAG3 binding to HspB8 and HspB6.

BAG3 (BCL2-associated athanogene 3) interacts with MMP-2 to positively regulate invasion by ovarian carcinoma cells.

BAG3 (BCL2-associated athanogene 3) is a member of the BAG family proteins, which interact with and regulate Hsp70. Our aim in the present study was to correlate BAG3 expression in ovarian cancer with invasion and progression-free survival. We found that BAG3 interacts with MMP2 in cultured ovarian cancer cells, and that knockdown of BAG3 expression downregulated MMP2 expression and diminished cell motility and invasiveness.

5-bromodeoxyuridine induces transcription of repressed genes with disruption of nucleosome positioning.

5-Bromodeoxyuridine (BrdU) modulates the expression of particular genes associated with cellular differentiation and senescence when incorporated into DNA instead of thymidine (dThd). To date, a molecular mechanism for this phenomenon remains a mystery in spite of a large number of studies. Recently, we have demonstrated that BrdU disrupts nucleosome positioning on model plasmids mediated by specific AT-tracts in yeast cells.

BAG3 and Hsc70 interact with actin capping protein CapZ to maintain myofibrillar integrity under mechanical stress.

Rationale: A homozygous disruption or genetic mutation of the bag3 gene, a member of the Bcl-2-associated athanogene (BAG) family proteins, causes cardiomyopathy and myofibrillar myopathy that is characterized by myofibril and Z-disc disruption. However, the detailed disease mechanism is not yet fully understood.

Objective: bag3(-/-) mice exhibit differences in the extent of muscle degeneration between muscle groups with muscles experiencing the most usage degenerating at an accelerated rate.

BAG3 directly associates with guanine nucleotide exchange factor of Rap1, PDZGEF2, and regulates cell adhesion.

BAG3, a member of the Hsc70 binding co-chaperone BAG-family proteins, has critical roles in regulating actin organization, cell adhesion, cell motility and tumor metastasis. The PDZ domain containing guanine nucleotide exchange factor 2 (PDZGEF2) was cloned as a BAG3-interacting protein. PDZGEF2 induces activation of Rap1 and increases integrin-mediated cell adhesion.