A case of a traumatic vertebral arteriovenous fistula associated with a hangman's fracture is reported. A 45-year-old male fell down about 2 meters and struck his parietooccipital region against the ground. Profuse nasal bleeding developed. He was transferred to a local hospital, where his respiration was ataxic and blood pressure was low. After intubation, he was transferred to our emergency department. Cervical x-p revealed fracture of C1, C2 and subluxation of C2 body. Because of uncontrollable nasal bleeding, the bilateral maxillary arteries were embolized with spongel. At this time, right vertebral angiograms demonstrated a vertebral arteriovenous fistula with an pseudoaneurysm located at C2 level. On the 13th hospital day, direct balloon occlusion of the fistula was attempted; this could not be achieved because the subclavian and vertebral arteries were tortuous and the balloon catheter could not be introduced to the level of the fistula in the vertebral artery. The patient was only observed until follow-up angiogram on the 24th hospital day revealed enlargement of the pseudoaneurysm. We performed trapping of both the proximal and distal ends of the involved vertebral artery; from C5 to C1. Postoperative course was uneventful, hangman's fracture was fixed with a Halo vest. Four months after operation, fistula and pseudoaneurysm were not opacified on angiogram. We believe that transvascular techniques are the treatment of choice for vertebral arteriovenous fistulas. However, as the next best thing, we can use trapping for the patient whose vessels are too tortuous to introduce the balloon catheter to the involved vessel.
Abstract microRNAs (miRNAs) regulate a wide variety of biological processes by silencing their target genes. Argonaute (AGO) proteins load miRNAs to form RNA-induced silencing complex (RISC), which mediates translational repression and/or mRNA decay of the targets. A scaffold protein called GW182 directly binds AGO and the CCR4-NOT deadenylase complex, initiating the mRNA decay reaction. Although previous studies have demonstrated the critical role of GW182 in cultured cells as well as in cell-free systems, its biological significance in living organisms remains poorly explored, especially in Drosophila melanogaster . Here, we generated gw182 -null flies using the CRISPR/Cas9 system and found that, unexpectedly, they can survive until an early second instar larval stage. Moreover, in vivo miRNA reporters can be effectively repressed in gw182 -null first instar larvae. Nevertheless, gw182 -null flies have defects in the expression of chitin-related genes and the formation of the larval trachea system, preventing them to complete the larval development. Our results highlight the importance of both GW182-dependent and -independent silencing mechanisms in vivo.
Tongues were removed from fetuses of mice on the 15th day of gestation (E15), from newborns (P0), and from juveniles on the 7th day (p7) and on the 21st day (P21) after birth for examination by light microscopy and transmission electron microscopy. In the fetuses at E15, no rudiments of filiform papillae were visible on the dorsal surface of the tongue. No evidence of keratinization was recognized throughout the entire dorsal lingual epithelium. At P0, rudiments of filiform papillae were compactly distributed over the dorsal surface, as are the filiform papillae in the adult, but their tips were rounder than those of the filiform papillae in the adult. Cell columns in the epithelium, with different degrees of keratinization of the type observed in the matured adult were indistinct. However, a keratinized layer was clearly visible on the tip of each filiform papilla. In juveniles at P7, the filiform papillae on the anterior part of the tongue were long and slender, and the anterior and posterior cell columns of the filiform papillae were identical to those in the adult. These results indicate that, in mice, the morphogenesis of filiform papillae advances in parallel with keratinization of the lingual epithelium from the stage just before birth to a stage a few weeks after birth.
Microporous layers (MPLs) applied to the catalyst layer (CL) side of the gas diffusion layer (GDL) of polymer electrolyte fuel cells have been developed to mitigate liquid water accumulation in the CL for oxygen transport to the cathode CL. A three-dimensional porous structure of our in-house hydrophobic MPL is numerically modeled with a pore network model (PNM). The convective air permeability and oxygen diffusivity, which depend on liquid saturation, are evaluated. To construct the PNM, focused ion beam scanning electron microscopy (FIB-SEM) is used to derive the pore size distribution. The model is ex-situ validated through air permeability and oxygen diffusivity tests with controlled saturation of non-volatile wetting liquid that is stable in the hydrophobic MPL. Oxygen diffusivity of the MPL is obtained by identifying the diffusion resistances of the concentration boundary layers and GDL substrate in the tests. The model predicts the effects of liquid water saturation in the MPL on the air and liquid water permeations, and the oxygen diffusion.
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Understanding buffering mechanisms for various perturbations is essential for understanding robustness in cellular systems. Protein-level dosage compensation, which arises when changes in gene copy number do not translate linearly into protein level, is one mechanism for buffering against genetic perturbations. Here, we present an approach to identify genes with dosage compensation by increasing the copy number of individual genes using the genetic tug-of-war technique. Our screen of chromosome I suggests that dosage-compensated genes constitute approximately 10% of the genome and consist predominantly of subunits of multi-protein complexes. Importantly, because subunit levels are regulated in a stoichiometry-dependent manner, dosage compensation plays a crucial role in maintaining subunit stoichiometries. Indeed, we observed changes in the levels of a complex when its subunit stoichiometries were perturbed. We further analyzed compensation mechanisms using a proteasome-defective mutant as well as ribosome profiling, which provided strong evidence for compensation by ubiquitin-dependent degradation but not reduced translational efficiency. Thus, our study provides a systematic understanding of dosage compensation and highlights that this post-translational regulation is a critical aspect of robustness in cellular systems.
Transfer RNA (tRNA) modifications are critical for protein synthesis. Queuosine (Q), a 7-deaza-guanosine derivative, is present in tRNA anticodons. In vertebrate tRNAs for Tyr and Asp, Q is further glycosylated with galactose and mannose to generate galQ and manQ, respectively. However, biogenesis and physiological relevance of Q-glycosylation remain poorly understood. Here, we biochemically identified two RNA glycosylases, QTGAL and QTMAN, and successfully reconstituted Q-glycosylation of tRNAs using nucleotide diphosphate sugars. Ribosome profiling of knockout cells revealed that Q-glycosylation slowed down elongation at cognate codons, UAC and GAC (GAU), respectively. We also found that galactosylation of Q suppresses stop codon readthrough. Moreover, protein aggregates increased in cells lacking Q-glycosylation, indicating that Q-glycosylation contributes to proteostasis. Cryo-EM of human ribosome-tRNA complex revealed the molecular basis of codon recognition regulated by Q-glycosylations. Furthermore, zebrafish qtgal and qtman knockout lines displayed shortened body length, implying that Q-glycosylation is required for post-embryonic growth in vertebrates.
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