Embedding of Laboratory Wastes in Clay or Concrete Blocks, with Special Reference to Baking Osmic Acid and Cacodylic Acid Wastes with Clay

Liquid laboratory waste containing osmic acid and cacodylic acid was mixed with potter's clay or hydraulic cement. The clay-waste product was kneaded into blocks and baked in a klin (1,200-1,400 degrees C). The cement-waste product was allowed to harden into concrete blocks. Some of the baked clay blocks and concrete blocks were ground, and immersed in 1 N NaOH or 10% HCI solutions for 3-6 months. X-ray microanalysis of the dried samples of these solutions showed that no leakage of osmium and arsenic occurred in the baked clay embedding, and that some leakage of these agents occurred in the concrete embedding. The present study indicates that the baked clay embedding method is useful for safe storage of dangerous laboratory wastes. Additional experiments suggested that glass embedding is also useful for safe storage of laboratory wastes or harmful metals.</p

Brefeldin A-inhibited guanine nucleotide-exchange protein 3 (BIG3) is predicted to interact with its partner through an ARM-type α-helical structure

Background: Brefeldin A-inhibited guanine nucleotide-exchange protein 3 (BIG3) has been identified recently as a novel regulator of estrogen signalling in breast cancer cells. Despite being a potential target for new breast cancer treatment, its amino acid sequence suggests no association with any well-characterized protein family and provides little clues as to its molecular function. In this paper, we predicted the structure, function and interactions of BIG3 using a range of bioinformatic tools. Results: Homology search results showed that BIG3 had distinct features from its paralogues, BIG1 and BIG2, with a unique region between the two shared domains, Sec7 and DUF1981. Although BIG3 contains Sec7 domain, the lack of the conserved motif and the critical glutamate residue suggested no potential guaninyl-exchange factor (GEF) activity. Fold recognition tools predicted BIG3 to adopt an α-helical repeat structure similar to that of the armadillo (ARM) family. Using state-of-the-art methods, we predicted interaction sites between BIG3 and its partner PHB2. Conclusions: The combined results of the structure and interaction prediction led to a novel hypothesis that one of the predicted helices of BIG3 might play an important role in binding to PHB2 and thereby preventing its translocation to the nucleus. This hypothesis has been subsequently verified experimentally

Electromagnetic spin polarization on the surface of topological insulator

We study the spin polarization of the electrons on the surface of topological insulators under a dc electric field or a circularly polarized light by using Keldysh Green's function formalism. When a dc electric field $E_x \sim 10^{3} {\rm V/m}$ is applied, a spin polarization $\simeq 5.2 \times 10^{-8}{\rm \AA^{-2}}$ is induced. Furthermore, we also find that a light illumination induces the out-of-plane component of the spin polarization as a result of the inverse Faraday effect. The magnitude of the spin polarization is proportional to the square of the lifetime $\tau$ and $\simeq 2 \times 10^{-10}{\rm \AA^{-2}}$ for typical parameters. Finally, we investigate the spin polarization in the presence of the warping term. By the symmetry consideration of the system, we find that the out-of-plane spin polarization is cubic of the current and that the magnitude of the induced spin polarization depends on the direction of the applied current.Comment: 10 pages, 6 figure

Early detachment of neuromuscular junction proteins in ALS mice with SODG93A mutation

The transgenic animals with mutant copper/zinc superoxide dismutase (SOD1) DNA develop paralytic motor neuron disease resembling human amyotrophic lateral sclerosis (ALS) patients and are commonly used as models for ALS. In the transgenic (Tg) mice with the G93A mutation of the human SOD1 gene SOD1G93A mice), the loss of ventral root axons and the synapses between the muscles and the motor neurons suggested that the motor neuron degeneration might proceed in a dying-back degeneration pattern. To reveal the relationship between axonal degeneration and the progression of the muscle atrophy in the SOD1G93A mice, we investigated the status of the neuromuscular junction along the disease progression. As a presynaptic or postsynaptic marker of neuromuscular junction (NMJ), anti-synaptic vesicle protein 2 (anti-SV2) antibody and α-bungarotoxin (α-BuTX) were chosen in this study and, as a marker of synaptic cleft, anti-agrin antibody was chosen in this study. In the immunohistochemistry of α-BuTX and anti-SV2 antibody, the percentages of double positive NMJs among α-BuTX single positive were decreased in Tg mice through time from ten weeks. The number of postsynaptic acethylcholine receptor (AChR) clusters did not decrease in Tg mice even at the end stage. Immunohistochemistry of α-BuTX and anti-agrin antibody revealed that the increase of immunopositive area of anti-agrin antibody around the muscle fiber in Tg mice from ten weeks of age. In this study, we revealed that the detachment of nerve terminals started at ten weeks in Tg mice. The levels of AChR did not change throughout 5–20 weeks of age in both groups of mice, and AChR remains clustering at NMJs, suggesting that the muscle abnormality is the result of detachment of nerve terminals

Functional interaction of hepatitis C virus NS5B with nucleolin GAR domain

金沢大学がん研究所Hepatitis C Virus (HCV) non-structural proteins are major components of replication complex that is modulated by several host factors. We previously reported that nucleolin, a representative nucleolar marker, interacts with the NS5B through two separated sequences, amino acids (aa) 208-214 and 500-506, and that W208 in the former stretch is essential for both nucleolin-binding and HCV replication. Here we evaluated the role of the latter stretch aa 500-506 of WRHRARS in nucleolin-binding and HCV replication scanned by alanine-substituted clustered mutant (cm) or point mutant (pm). One tryptophan and three arginine residues in the sequence were found to be essential both for nucleolin-binding in vivo and HCV replication detected with a HCV subgenomic replicon transfected into Huh7 cells. NS5B-binding of nucleolin was further delineated by truncation and clustered mutants of nucleolin. Arginine-glycine-glycine (RGG) repeat in the Glycine arginine rich (GAR) domain were defined to be indispensable for NS5B-binding immunologically detected in in vivo and in vitro although short internal-truncations of RGG repeat are tolerable for NS5B-binding. These results indicate that nucleolin is a critical host factor for HCV replication through the direct interaction between W208 and several residues at the sequence, aa 500-505, of NS5B, and the long-turn motif including RGG repeat at nucleolin C-terminal. © 2007 The Japanese Biochemical Society

Changes in aniseikonia and influencing-factors following successful macula-off retinal detachment surgery

This study investigated the changes in the severity of aniseikonia after surgery for macula-off retinal detachment (RD), and the relationship between aniseikonia and retinal microstructures. The study included 26 eyes of 26 patients undergoing RD surgery. Visual acuity was measured preoperatively, and at 3, 6, and 12 months postoperatively. Degree of aniseikonia and OCT images were obtained at 3, 6, and 12 months postoperatively. The aniseikonia values (mean +/- standard deviation) at 3, 6, and 12 months postoperatively were -5.3 +/- 4.2%, -4.4 +/- 4.4%, and -3.1 +/- 3.2%, respectively. Significant improvement was observed from 3 to 12 months postoperatively (P = 0.001). Twelve months postoperatively, 14 eyes had micropsia, 1 eye had macropsia, and 11 eyes were free of aniseikonia. Stepwise multiple regression analyses revealed that the severity of aniseikonia at 12 months postoperatively was significantly associated with postoperative development of cystoid macular edema (CME) and epiretinal membrane (ERM), as well as area of preoperative RD. In conclusion, although aniseikonia was gradually relieved after RD surgery during a 1-year follow-up period, approximately half of patients had aniseikonia and almost all of them had micropsia. Aniseikonia was associated with presence of postoperative CME, ERM, and area of preoperative RD

Pancreatic Duct-to-mucosa versus Invagination or Complete External Drainage Anastomosis in Case of Small Pancreatic Duct after Pancreaticoduodenectomy: Comparative Historical Review

After pancreaticoduodenectomy (PD), pancreatic duct-to-mucosa anastomosis (PDM) has been usually applied which may prevent risk of pancreatic fistula (PF). In cases with a small pancreatic duct, however, PDM is difficult to complete. Procedures involving the invagination (IV) or complete external tube drainage (CED) are supposed to be alternative options for anastomosis. We retrospectively compared clinical results between PDM and IV or CED in 104 patients with a tiny pancreatic duct who underwent PD. The 77 patients undergoing PDM (the control group) and 27 patients undergoing other procedures, including 19 for CED and 8 for IV, were comparatively examined. Fatty pancreas was commonly observed in CED group. Pancreaticojejunostomy was significantly more frequently applied in CED group, and the operating time in the IV group was significantly longer than in control group (p<0.05). The anastomotic time in CED group tended to be shorter than those in control and IV groups (18 versus 29 and 37 min). The incidences of PF were not significantly different among groups (31% in control, 47% inCED and 14% in IV, respectively); however, a grade B or C level of PF was not observed in the IV group. PDM is often difficult to achieve and inadequate suturing may injure the pancreatic parenchyma in cases of very small pancreatic duct. Re-evaluation of the CED or IV procedure as an alternative option was suggested to be warranted

ALS mutations in FUS cause neuronal dysfunction and death in Caenorhabditis elegans by a dominant gain-of-function mechanism.

It is unclear whether mutations in fused in sarcoma (FUS) cause familial amyotrophic lateral sclerosis via a loss-of-function effect due to titrating FUS from the nucleus or a gain-of-function effect from cytoplasmic overabundance. To investigate this question, we generated a series of independent Caenorhabditis elegans lines expressing mutant or wild-type (WT) human FUS. We show that mutant FUS, but not WT-FUS, causes cytoplasmic mislocalization associated with progressive motor dysfunction and reduced lifespan. The severity of the mutant phenotype in C. elegans was directly correlated with the severity of the illness caused by the same mutation in humans, arguing that this model closely replicates key features of the human illness. Importantly, the mutant phenotype could not be rescued by overexpression of WT-FUS, even though WT-FUS had physiological intracellular localization, and was not recruited to the cytoplasmic mutant FUS aggregates. Our data suggest that FUS mutants cause neuronal dysfunction by a dominant gain-of-function effect related either to neurotoxic aggregates of mutant FUS in the cytoplasm or to dysfunction in its RNA-binding functions