Cloning of CRP2, a novel member of the cysteine-rich protein family with two repeats of an unusual LIM/double zinc-finger motif

AbstractThe cDNA coding for a novel member of the cysteine-rich protein family was isolated from a rat brain cDNA library. It encodes a protein, denoted cysteine-rich protein 2 (CRP2), of 208 amino acid residues containing two tandem repeats of an unusual LIM/double zinc-finger-like motif. The ubiquitous tissue distribution and high level of expression of CRP2 mRNA suggest an important role for CRP2 in cell functions

Comparison of FGF1 (aFGF) Expression between the Dorsal Motor Nucleus of Vagus and the Hypoglossal Nucleus of Rat

Neurons in the dorsal motor nucleus of the vagus (DMNV) are more severely affected by axonal injury than most other nerves, such as those of the hypoglossal nucleus. However, the mechanism underlying such a response remains unclear. In this study, we compared the expression of fibroblast growth factor 1 (FGF1), a neurotrophic factor, between the DMNV and the hypoglossal nucleus by RT-PCR and immunohistochemical analyses. RT-PCR showed that the level of FGF1 mRNA expression in the DMNV was lower than that in the hypoglossal nucleus (P<0.01). Immunohistochemistry revealed that FGF1 was localized to neurons. FGF1-positive neurons in large numbers were evenly distributed in the hypoglossal nucleus, whereas FGF1-positive neurons were located in the lateral part of the DMNV. Double immunostaining for FGF1 and choline acetyltransferase demonstrated that 22.7% and 78% of cholinergic neurons were positive for FGF1 in the DMNV and hypoglossal nucleus, respectively. A tracing study with cholera toxin B subunit (CTb) demonstrated that cholinergic neurons sending their axons from the DMNV to the superior laryngeal nerve were FGF1-negative. The results suggest that the low expression of FGF1 in the DMNV is due to severe damage of neurons in the DMNV

Effects of Sciatic Neurectomy on Arthritis and Bone Loss in Rats with Collagen-Induced Arthritis

We investigated the effects of sciatic neurectomy on arthritis and bone mineral density (BMD) in 7-month-old female Sprague-Dawley rats with collagen-induced arthritis (CIA). After the animals obtained a uniform mean body weight, we divided them at random into 4 groups, and treated them with the following surgical manipulations: (i) sham group (n = 8), sham surgery; (ii) CIA group (n = 9), collagen sensitization and sham surgery; (iii) NTx group (n = 9), sciatic neurectomy and (iv) CIA + NTx group (n = 9), collagen sensitization and a sciatic neurectomy. Every 2 weeks up to 8 weeks after sensitization, the arthritis score for hind paw swelling was evaluated, and BMD of the cancellous and cortical bones in the proximal tibia was measured by peripheral quantitative computed tomography (pQCT). Both the hind paw swelling and arthritis score in the CIA + NTx group were significantly lower than those in the CIA group at 6 and 8 weeks after sensitization. There was no significant difference in the cancellous BMD between the CIA and CIA + NTx groups. The cortical BMD of the tibial metaphysis was significantly lower in the NTx and CIA + NTx groups than in the sham group at 4 and 8 weeks, and in the CIA + NTx group than in the CIA group at 4 weeks after sensitization. There was no significant difference between the CIA and sham groups as well as the CIA and CIA + NTx group at 8 weeks after sensitization. It was concluded that sciatic neurectomy suppressed the severity of arthritis, but did not affect the cancellous bone loss in adult CIA rats

Role of the silkworm argonaute2 homolog gene in double-strand break repair of extrachromosomal DNA

The argonaute protein family provides central components for RNA interference (RNAi) and related phenomena in a wide variety of organisms. Here, we isolated, from a Bombyx mori cell, a cDNA clone named BmAGO2, which is homologous to Drosophila ARGONAUTE2, the gene encoding a repressive factor for the recombination repair of extrachromosomal double-strand breaks (DSBs). RNAi-mediated silencing of the BmAGO2 sequence markedly increased homologous recombination (HR) repair of DSBs in episomal DNA, but had no effect on that in chromosomes. Moreover, we found that RNAi for BmAGO2 enhanced the integration of linearized DNA into a silkworm chromosome via HR. These results suggested that BmAgo2 protein plays an indispensable role in the repression of extrachromosomal DSB repair

ハイ アスペルギローマ ジュツゴ ハイロウ ニ タイシテ PushampSlideホウ ト ロープウェイホウ オ オウヨウ シタ EWS ニヨル キカンシ ジュウテンジュツ ガ ユウヨウ デアッタ 1レイ

Background : Bronchial occlusion using endobronchial Watanabe Spigot（EWS）is reported to be useful for treatment of secondary intractable pneumothorax and thoracic empyema, peripheral bronchial fistula. However, the methods of the bronchial occlusion are sometimes difficult and EWS sometimes fall off from plugged bronchus. Case : A ４４ year old man presented hemosputum. He was diagnosed with Aspergilloma. We performed a resection of the right upper lobe and S６ partial resection. Air leak appeared at postoperative day ３. We performed EWS embolization with an application of push & slide method and the ropeway method, and the persistent air leak disappeared. Conclusion : Our method is useful when the bronchial occlusion is difficult

RNA-Binding Protein Musashi1 Modulates Glioma Cell Growth through the Post-Transcriptional Regulation of Notch and PI3 Kinase/Akt Signaling Pathways

Musashi1 (MSI1) is an RNA-binding protein that plays critical roles in nervous-system development and stem-cell self-renewal. Here, we examined its role in the progression of glioma. Short hairpin RNA (shRNA)-based MSI1-knock down (KD) in glioblastoma and medulloblastoma cells resulted in a significantly lower number of self renewing colony on day 30 (a 65% reduction), compared with non-silencing shRNA-treated control cells, indicative of an inhibitory effect of MSI1-KD on tumor cell growth and survival. Immunocytochemical staining of the MSI1-KD glioblastoma cells indicated that they ectopically expressed metaphase markers. In addition, a 2.2-fold increase in the number of MSI1-KD cells in the G2/M phase was observed. Thus, MSI1-KD caused the prolongation of mitosis and reduced the cell survival, although the expression of activated Caspase-3 was unaltered. We further showed that MSI1-KD glioblastoma cells xenografted into the brains of NOD/SCID mice formed tumors that were 96.6% smaller, as measured by a bioluminescence imaging system (BLI), than non-KD cells, and the host survival was longer (49.3±6.1 days vs. 33.6±3.6 days; P<0.01). These findings and other cell biological analyses suggested that the reduction of MSI1 in glioma cells prolonged the cell cycle by inducing the accumulation of Cyclin B1. Furthermore, MSI1-KD reduced the activities of the Notch and PI3 kinase-Akt signaling pathways, through the up-regulation of Numb and PTEN, respectively. Exposure of glioma cells to chemical inhibitors of these pathways reduced the number of spheres and living cells, as did MSI1-KD. These results suggest that MSI1 increases the growth and/or survival of certain types of glioma cells by promoting the activation of both Notch and PI3 kinase/Akt signaling