Effect of Using a Cardiac Catheterization Table-Stabilizing Stick on the Quality of Cardiopulmonary Resuscitation in the Cardiac Catheterization Laboratory: A Simulation-Based Study.

Rapid defibrillation and high-quality cardiopulmonary resuscitation (CPR) are necessary for patients with cardiopulmonary arrest, one of the most serious and frequently encountered complications in cardiac catheterization laboratories. However, when the catheterization table is withdrawn from its neutral position for fluoroscopy, it is unstable and unsuitable for resuscitation because of its cantilever structure. To stabilize the table in its withdrawn position, the use of a table-stabilizing stick might improve CPR quality. To investigate the effect of using a cardiac catheterization table-stabilizing stick on CPR quality, a CPR simulation mannequin was placed on a cardiac catheterization table that was withdrawn from the C-arm of the X-ray machine. CPR quality was assessed with or without the use of a table-stabilizing stick under the table. The CPR quality assessment (Q-CPR) scores were 79.6 ± 11.4% using the table-stabilizing stick and 47.7 ± 30.3% without the use of the stick device (p = 0.02). In this simulation-based study, the use of a table-stabilizing stick in a cardiac catheterization table withdrawn from the C-arm of the X-ray machine improved the quality of CPR.

Characterization of Russell bodies accumulating mutant antithrombin derived from the endoplasmic reticulum.

The endoplasmic reticulum (ER) adjusts its size and architecture to adapt to change in the surrounding environment. Russell bodies (RBs) were originally described as dilated structures of the ER cisternae containing large amounts of mutant immunoglobulin. Similar structures are observed in a wide variety of mutant proteins accumulated in the ER. We previously prepared Chinese hamster ovary (CHO) cells in which the expression of mutant antithrombin (AT) (C95R) was controlled with a Tet-On system and showed that RBs can be conditionally formed. However the precise architecture and intracellular behavior of RBs have been as yet only poorly characterized. To characterize the properties of RB, we prepared the same system using a green fluorescent protein (GFP)-fused mutant and measured the dynamics and architecture of RBs. We observed the mobile nature of the molecule in the RB lumen and RBs were separated from the rest of the ER network by narrow tubes. Furthermore, we found that the RBs were not simply expanded ER membranes. The RB lumen is filled with misfolded proteins that are surrounded by ER membranes. In addition, RBs mostly maintain their structure during cell division, possess ribosomes on their membranes and synthesize AT(C95R)-GFP. Based on the characterization of the hydrodynamic radius of AT(C95R)-GFP and the effect of DP1, an ER-shaping protein, we propose that RBs are spontaneously formed as a result of the partitioning of the misfolded AT with the shaping protein.

Endoplasmic Reticulum Stress Response and Mutant Protein Degradation in CHO Cells Accumulating Antithrombin (C95R) in Russell Bodies.

Newly synthesized secretory proteins are folded and assembled in the endoplasmic reticulum (ER), where an efficient protein quality control system performs a critically important function. When unfolded or aggregated proteins accumulate in the ER, certain signaling pathways such as the unfolded protein response (UPR) and ER-overload response (EOR) are functionally active in maintaining cell homeostasis. Recently we prepared Chinese hamster ovary (CHO) cells expressing mutant antithrombin (AT)(C95R) under control of the Tet-On system and showed that AT(C95R) accumulated in Russell bodies (RB), large distinctive structures derived from the ER. To characterize whether ER stress takes place in CHO cells, we examined characteristic UPR and EOR in ER stress responses. We found that the induction of ER chaperones such as Grp97, Grp78 and protein disulfide isomerase (PDI) was limited to a maximum of approximately two-fold. The processing of X-box-binding protein-1 (XBP1) mRNA and the phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) subunit were not induced. Furthermore, the activation of nuclear factor-kappa B (NF-κB) was not observed. In contrast, CHO cells displayed UPR and EOR when the cells were treated with thapsigargin and tumor necrosis factor (TNF)-α, respectively. In addition, a portion of the mutant AT(C95R) was degraded through proteasomes and autophagy. CHO cells do respond to ER stress but the folding state of mutant AT(C95R) does not appear to activate the ER stress signal pathway.

Analysis of the expression of candidate genes for type 1 diabetes susceptibility in T cells.

Type 1 diabetes is characterized by T-cell-mediated autoimmune destruction of pancreatic ß-cells. Currently, approximately 50 type 1 diabetes susceptibility genes or chromosomal regions have been identified. However, the functions of type 1 diabetes susceptibility genes in T cells are elusive. In this study, we evaluated the correlation between type 1 diabetes susceptibility genes and T-cell signaling. The expression levels of 22 candidate type 1 diabetes susceptibility genes in T cells from nonobese diabetic (NOD), control C57BL/6 (B6), and NOD-control F1 hybrid mice were analyzed in response to 2 key immunoregulatory cytokines: interleukin-2 (IL-2) and transforming growth factor ß (TGF-ß). Exogenous gene expression studies were also performed in EL4 and Jurkat E6.1 T-cell lines. Significant differences in the expression of Clec16a, Dlk1, Il2, Ptpn22, Rnls, and Zac1 (also known as Plagl1) were observed in T cells derived from the 3 strains of mice, and TGF-ß differentially influenced the expression of Ctla4, Foxp3, Il2, Ptpn22, Sh2b3, and Zac1. We found that TGF-ß induced Zac1 expression in both primary T cells and EL4 cells and that exogenous expression of Zac1 and ZAC1 in T-cell lines altered the expression of Il2 and DLK1, respectively. The results of our study indicate the possibility that additional genetic pathways underlying type 1 diabetes susceptibility, including those involving Clec16a, Dlk1, Rnls, Sh2b3, and Zac1 under IL-2 and TGF-ß signaling in T cells, may be shared between human and NOD mice.

Effects of Land Use Changes from Paddy Fields on Soil Bacterial Communities in a Hilly and Mountainous Area.

Soil bacterial community structures in terraced rice fields and abandoned lands in a hilly and mountainous area were analyzed using 16S rRNA gene sequences. The DGGE band patterns of each soil were similar. Based on pyrosequencing data, the richness and diversity of bacterial species were slightly higher in paddy fields than in other soils. A beta-diversity analysis clearly indicated that the bacterial community structure in paddy fields differed from those in non-paddy field lands and crop fields that had not been used as a paddy field. These results may reflect the history of land use.